Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Contact lens materials over the last 20 years have progressed from polymethyl methacrylate (PMMA) through hydrogels to high Dk rigid and semi-soft lenses. Our understanding of how and why contact lenses affect the eye has also advanced considerably. We now know that: (1) the oxygen demands of the eye are high and (2) carbon dioxide accumulates and corneal acidosis occurs with most current contact lenses, especially with extended wear (EW). The effects of these perturbations on the epithelium include decreased metabolic rate, thinning, microcysts, and reduced adhesion. In addition, stromal edema and thinning and, with pressure, distortion occur with the long-term use of low to moderate oxygen transmissible lenses. Endothelial polymegethism also occurs and is a relatively permanent effect of inadequate oxygen permeability (Dk). The major consequence of chronic hypoxia and acidosis is, for a significant number of patients, corneal intolerance and discontinuation of lens wear. High permeability materials (100 Dk) that provide adequate gaseous exchange for daily wear and minimal changes in EW are now available and should be used where possible. The more obvious problems of contact lens-induced chronic inflammation, e.g., contact lens-induced papillary conjunctivitis (CLPC), and acute inflammation, e.g., acute red eye (ARE), are less well understood. Protein deposits, lens ageing, occlusion, mechanical effects, and bacterial contamination have all been implicated. The remaining frontiers include understanding and avoiding the stimuli to low grade irritation and inflammation by making contact lenses more comfortable and improving their compatibility with the ocular surfaces.
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PMID:The Glenn A. Fry Award lecture 1988: the ocular response to contact lens wear. 251 6

Twenty-six patients with metastatic colorectal adenocarcinoma were entered into a Phase I-II study of 5-fluorouracil (5-FUra)-high-dose leucovorin (CF). The starting dose of 5-FUra was 300 mg/sq m with escalation to 750 mg/sq m/week in 6 doses given by rapid i.v. injection midway during a 2-hr infusion of CF, 500 mg/sq m. Partial responses were seen in 9 of 23 patients (6 of 12 who had had previous 5-FUra). Complete normalization of liver enzymes was seen in two of these patients. Side effects were seen sporadically with 5-FUra doses up to 600 mg/sq m. At a 600-mg/sq m 5-FUra dose, 8 of 18 patients had diarrhea, and 2 of 18 had white blood cell counts less than 3000/microliter. At a 750-mg/sq m dose of 5-FUra, 6 of 11 patients had severe diarrhea and 6 of 11 had white blood cell counts less than 3000/microliter. Other toxicities were mild conjunctivitis and lacrimation, thinning of the nails, and alopecia. In bioavailability studies of CF p.o., no plasma CF could be detected. After CF i.v., mean plasma peak was 111.3 +/- 40.3 (S.D.) microM. 5-FUra-CF appears to be effective in patients clinically resistant to 5-FUra. This study is being extended to randomized trial of 5-FUra-CF versus 5-FUra alone.
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PMID:Phase I-II trial of high-dose calcium leucovorin and 5-fluorouracil in advanced colorectal cancer. 633 82

In patients who have graft-vs-host disease (GVHD) after bone marrow transplantation, ocular involvement occurs in approximately 60% of cases. Among 13 such GVHD patients, the most frequent ocular manifestations included keratoconjunctivitis sicca, cicatricial lagophthalmos, and sterile conjunctivitis and uveitis. The severe ocular complications of persistent corneal epithelial defects and both noninfected and infected stromal ulceration were related to the concomitant dry-eye condition and could be managed by conventional therapy including topical lubricants and antibiotics, punctal occlusion, bandage soft contact lenses, tarsorrhaphy, tissue adhesive, conjunctival flap, and conjunctival homograft. Postmortem and surgical tissues from four patients revealed conjunctival and corneal epithelial thinning and keratinization, lacrimal inspissation without inflammatory infiltration, and diffuse choroiditis. Keratoconjunctivitis sicca in GVHD patients might be a combined result of drug toxicity effects and GVHD. The frequent and potentially severe ocular problems in these patients suggest that close ophthalmic monitoring is mandatory in bone marrow transplant recipients.
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PMID:Ocular manifestations of graft-vs-host disease. 633 37

Repeated topical applications of fluoresceinyl ovalbumin (FL-OA) to the conjunctival sac of guinea pigs sensitized them for conjunctival type 1 hypersensitivity reactions and mast cell degranulation. Guinea pigs infected with Ascaris suum, with high titers of circulating anti-A suum IgE and IgG1 antibody, also produced conjunctival type 1 reactions on topical challenge with A suum antigen. These reactions were no more intense than those of animals topically sensitized and challenged with FL-OA, which in some instances had no detectable serum homocytotropic antibody. Persistently reactive animals that had undergone repeated type 1 conjunctival reactions had histological findings (eg, papillary changes with extensive epithelial eosinophil infiltrates, epithelial thickening or thinning, numerous goblet cells, subepithelial lymphoid cell infiltrates, and new vessel formation) resembling those of human atopic vernal conjunctivitis.
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PMID:Vernal conjunctivitis. Model studies in guinea pigs immunized topically with fluoresceinyl ovalbumin. 649 52

Ulcerative colitis (Crohn's disease) is a chronic relapsing inflammatory bowel disease of unknown etiology. The most common ocular complications include conjunctivitis and uveitis, particularly iritis. Herein, we describe a patient who had a decrease in visual acuity due to an increasing astigmatism. This was accompanied with a peripheral limbal thinning of the cornea and faint confluent corneal changes. No systemic activity was present during the period that the patient was monitored. Changes of astigmatism were followed up with videokeratography. This apparatus monitors changes in clinical course accurately and makes comparison possible between separate visits.
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PMID:Crohn's colitis and the cornea. 907 38

Trachoma is a leading cause of preventable blindness worldwide. The disease is caused by an intracellular epithelial gram-negative bacterium, Chlamydia trachomatis. The presence of children, overcrowding, and the lack of water in the household are factors that predispose to the transmission of the disease. The disease may remain asymptomatic but some patients many complain of redness, irritation, and ocular discharge. The principal initial clinical manifestation is a follicular conjunctivitis that may lead to conjunctival scarring, entropion, trichiasis, corneal thinning, and ulceration. Some patients develop corneal scars that lead to loss of vision. Despite the remarkable progress in our understanding of Chlamydial infections, the basic mechanisms involved in tissue damage and scarring remain to be elucidated. There are several effective therapeutic modalities for trachoma. Azithromycin oral single dose was found to be safe and effective in children with active trachoma. Conjunctival biopsy specimens obtained from adult patients receiving a single oral dose of azithromycin showed sustained high levels of azithromycin (above MIC of chlamydia) for up to 2 weeks after intake. These prolonged high levels of azithromycin in the conjunctival tissue following a single oral dose makes the drug suitable for the treatment of endemic trachoma.
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PMID:Trachoma: a review. 1143 24

A 15-year-old boy presented with left-sided ptosis, upper eyelid swelling, proptosis, conjunctivitis, and a central corneal epithelial defect with thinning. MRI demonstrated an enhancing orbital mass associated with the lacrimal gland. Biopsy findings were consistent with orbital inflammatory syndrome. Topical cyclosporine and 1% methylprednisolone eliminated the anterior segment inflammation; subsequent treatment with systemic prednisone reduced the ptosis and edema. To our knowledge, this is the only reported case of orbital inflammatory syndrome associated with a corneal epithelial defect and thinning.
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PMID:Corneal melt associated with idiopathic dacryoadenitis. 1723 95

Aerosolized medications maximize clinical benefit by targeting the airways and minimize side effects by reducing (though not eliminating) systemic exposure. Aerosolized drugs delivered with a facemask may inadvertently deposit on the face and in the eyes, raising concerns about cutaneous and ocular side effects with these drugs. Cases of anisocoria have been reported from exposure of the eyes to aerosol bronchodilators. Whether inhaled corticosteroids (ICS) can cause skin and eye problems like those seen with systemic or topical steroids is more difficult to answer. Patients who take ICS may have other corticosteroid exposures, or have other conditions that predispose them to side effects, making the analysis of the ICS risk challenging. Also, many studies were not designed to search for cutaneous or ocular effects, or may have been too short to detect these effects. Nevertheless, ICS have been associated with an increased risk of skin thinning, bruising, cataracts and possibly glaucoma in adults, but not in children. The risks increase with advanced age, higher doses, and longer duration of use. In children, the risks of cataracts and glaucoma were negligible with ICS, whether a mouthpiece or a mask interface was used. Side effects like skin rash and conjunctivitis occurred at low frequencies similar to placebo or comparator drugs. We do not know whether exposed children will have increased risks from ICS later in life. Therefore, it is wise to avoid face and eye deposition when possible, and to use the minimally effective dose.
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PMID:Clinical side effects during aerosol therapy: cutaneous and ocular effects. 1741 1

Ocular infection with HSV-1 continues to be a serious clinical problem despite the availability of effective antivirals. Primary infection with HSV-1 can involve ocular and adenaxial sites and can manifest as blepharitis, conjunctivitis, or corneal epithelial keratitis. After initial ocular infection, HSV-1 can establish latent infection in the trigeminal ganglia for the lifetime of the host. During latency, the viral genome is retained in the neuron without producing viral proteins. However, abundant transcription occurs at the region encoding the latency-associated transcript, which may play significant roles in the maintenance of latency as well as neuronal reactivation. Many host and viral factors are involved in HSV-1 reactivation from latency. HSV-1 DNA is shed into tears and saliva of most adults, but in most cases this does not result in lesions. Recurrent disease occurs as HSV-1 is carried by anterograde transport to the original site of infection, or any other site innervated by the latently infected ganglia, and can reinfect the ocular tissues. Recurrent corneal disease can lead to corneal scarring, thinning, stromal opacity and neovascularization and, eventually, blindness. In spite of intensive antiviral and anti-inflammatory therapy, a significant percentage of patients do not respond to chemotherapy for herpetic necrotizing stromal keratitis. Therefore, the development of therapies that would reduce asymptomatic viral shedding and lower the risks of recurrent disease and transmission of the virus is key to decreasing the morbidity of ocular herpetic disease. This review will highlight basic HSV-1 virology, and will compare the animal models of latency, reactivation, and recurrent ocular disease to the current clinical data.
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PMID:Ocular HSV-1 latency, reactivation and recurrent disease. 1858 63

Relapsing polychondritis (RP) is a rare systemic autoimmune disease characterized by episodic inflammation of cartilaginous tissues throughout the body. It is distinguished by recurrent bouts of inflammation, which lead to the permanent destruction of the involved structures. It can be a life-threatening, debilitating, and frightening disease and is often difficult to diagnose in its early stages. Ocular manifestations have been reported to occur in up to 65% of cases and include proptosis, eyelid edema, extraocular muscles palsy, episcleritis, scleritis, conjunctivitis, corneal infiltrate, peripheral ulcerative keratitis, corneal thinning or perforation, iridocyclitis, cataract, retinopathy, exudative retinal detachment, and optic neuritis. Corticosteroids remain the mainstay of treatment for RP; however, other treatment modalities include nonsteroidal anti-inflammatory drugs, colchicine, dapsone, and immunomodulatory drugs. This article reviews the literature and summarizes the epidemiology, pathogenesis, clinical features, treatment, and prognosis of the systemic and ocular manifestations of RP.
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PMID:Relapsing polychondritis: systemic and ocular manifestations, differential diagnosis, management, and prognosis. 2195 72


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