Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of an 8-year-old girl with immune ring is presented. Immune reaction in the cornea after the second assault of the same antigen, probably HSV, produced immuno-complexes deposited in the cornea as a ring-shaped lattice. In our case the girl was admitted to hospital because of blurred vision, corneal deposits in the shape of a ring with keratomycosis suspicion in the eye. 3 months before she suffered from a minor injury to this eye (corneal abrasion with a finger while playing). Immune ring was recognised. Following Missoten's recommendations the girl was treated mainly with topical steroids (ophticor) every 15 minutes on the first day until the afternoon, subsequently with dexamethasone 4 times a day--for 10 days with decreased frequency continuously in an amount stopping the immune reaction. After 3 days the regression of deposits and the visual acuity improved. I believe this disease is not rare but rarely recognised and my aim is to approach this problem more thoroughly.
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PMID:[A case of a patient with immune ring of cornea]. 1093 98

Autosomal dominant granular corneal dystrophy is a stromal corneal dystrophy characterized by discrete granular opacities that cause recurrent corneal erosion and blurred vision. Four different corneal dystrophies, including granular dystrophy, are caused by mutations of the BIGH3 gene. We report a case of autosomal dominant granular corneal dystrophy in a 45-year-old woman with bilateral blurred vision and recurrent eye pain since adolescence. Numerous diffuse granular opacities were found in the superficial stroma of the cornea. Her 3 sons had a similar history and clinical presentation. Autosomal dominant granular corneal dystrophy was diagnosed. Mutation analysis by single-strand conformation polymorphism and direct sequencing in 2 of the affected family members revealed R555W mutation in the BIGH3 gene. This independent R555W mutation has been previously found in different ethnic populations including Caucasians and Japanese with granular dystrophy of Groenouw type I. These findings indicate the importance of R555 amino acid in the pathogenesis of autosomal dominant granular corneal dystrophy.
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PMID:An autosomal dominant granular corneal dystrophy family associated with R555W mutation in the BIGH3 gene. 1270 42

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

A 33-year-old woman had progressive blurred vision 2 weeks after uneventful laser in situ keratomileusis surgery. Initial satisfactory uncorrected visual acuity (UCVA) was complicated by postoperative dry eye and drug toxicity. Slitlamp biomicroscopy revealed diffuse punctate epithelial keratitis and inferior corneal epithelial defect with rolled-up epithelium on the flaps and the inferior unoperated cornea in both eyes. Diffuse inflammatory cell infiltrates were evident in the stroma. Stromal thinning was evident on serial Orbscan (Bausch & Lomb) and pachymetry examinations, and a hyperopic shift of almost +6 diopters was observed in the refractive error in both eyes. These examinations showed a gradual recovery of stromal thickness after copious hydration with balanced salt solution. The UCVA was 1.0 in both eyes after corneal rehydration.
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PMID:Toxic keratopathy-related corneal dehydration after laser in situ keratomileusis. 1612 7

We report on the confocal microscopical findings of both corneas of a patient presenting a multiple myeloma associated crystalline keratopathy and the response to treatment. Blurred vision was the first sign of progression of the multiple myeloma. Confocal microscopy images show needle-like structures in the epithelium and stroma of the cornea which regressed after treatment of the multiple myeloma.
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PMID:Confocal microscopy in multiple myeloma associated crystalline keratopathy: case report. 1690 7

Bee stings of the cornea are rarely reported, but have the potential for causing serious ophthalmological injuries. We present a case of corneal bee sting with retained stinger apparatus. A 35-year-old patient presented with an acute, corneal bee sting of the right eye 12 hours after he was stung. The patient suffered from pain, blurred vision, and epiphora. The right eye showed edema of the upper and lower eyelid, conjunctival hyperemia, chemosis, and striate keratitis of the paracentral cornea by biomicroscopic examination. The stinger was identified in the depth of the corneal infiltration. Visual acuity was 5/10. It was removed surgically. After 2 months, the eye only showed a minimal residual corneal opacification. Visual acuity was 10/10. We present a case of bee sting to the cornea with retained stinger apparatus and treatment of this unusual presentation.
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PMID:Bee sting of the cornea: a case study and review of the literature. 1720 May 91

Phenothiazines can give rise to serious and sometimes irreversible dermatological and oculotoxic side effects. These effects can take the form of photosensitivity, grey-purple discoloration and hyperpigmentation of the skin and hyperpigmentation of the conjunctiva, cornea, lens, retina, choroidea and macula. Involvement of the retina or macula can lead to impaired vision, blurred vision, disturbed colour perception and night blindness. We describe the mechanisms that are currently believed to underlie these side-effects. We advise annual ophthalmic monitoring of patients receiving long-term treatment with phenothiazianes.
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PMID:[Oculotoxic and dermatotoxic side effects of phenothiazines]. 1743 11

Ophthalmic drug delivery is one of the most interesting and challenging endeavors facing the pharmaceutical scientist. The conventional ocular drug delivery systems like solutions, suspensions, and ointments show drawbacks such as increased precorneal elimination, high variability in efficiency, and blurred vision respectively. In situ-forming hydrogels are liquid upon instillation and undergo phase transition in the ocular cul-de-sac to form visco-elastic gel and this provides a response to environmental changes. In the past few years, an impressive number of novel temperature, pH, and ion induced in situ-forming systems have been reported for sustain ophthalmic drug delivery. Each system has its own advantages and drawbacks. The choice of a particular hydrogel depends on its intrinsic properties and envisaged therapeutic use. This review includes various temperature, pH, and ion induced in situ-forming polymeric systems used to achieve prolonged contact time of drugs with the cornea and increase their bioavailability.
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PMID:In situ-forming hydrogels for sustained ophthalmic drug delivery. 2365 Jun 62

Although many factors that trigger the herpes simplex virus (HSV) reactivation from latency have been reported, how HSV resides in a latent state in the normal human cornea still needs to be defined. We therefore conducted a series of studies regarding various aspects of HSV infections. To understand how patients subjectively perceived changes in their daily life that could have induced HSV reactivation, we first performed a comprehensive survey on the subjective factors in patients who had experienced recurrent herpetic keratitis. The result of our survey revealed that stress, lack of sleep, shoulder stiffness, and physical fatigue were the key factors. There were various causes for stress, and stress associated with reactivation often occurred between spring and summer. Regarding HSV latency in the normal cornea, we used real-time polymerase chain reaction (PCR) to determine the presence of HSV in the donor and host corneas. The findings showed that on average, those host corneas with a history of HSV keratitis had 1.6 x 10(4) copies/mg of HSV DNA, while the host corneas without a history and the donor corneas had 8.7 and 4.9 x 10(2) copies/mg of HSV DNA, respectively. Based on these observations, it is reasonable to infer that latent viruses could have resided in a normal cornea without a history and were transmitted to a host cornea through corneal transplantation. We also quantified the virus load in tears before and after ocular surgery (one week after corneal transplantation or the next day after vitreous surgery). Our results indicated that both the detection rate and the average copy number of HSV DNA had a tendency to increase postperatively. Moreover, we tried to differentiate the HSV strains that were involved in the recurrent lesions. In only one of the studied cases, could we find a single different nucleotide between two HSV strains. It seemed possible that two different strains of HSV had set off the same episode of reactivation. In recent years, chemokines have become known for their action in mediating inflammatory diseases. We suspected that chemokines might also play a role in the antiviral mechanism and examined the chemokine-derived antiviral activity. We used eight chemokines, including RANTES/CCL5, MIP-lalpha/ CCL3, and MIP-1beta/CCL4, in a murine HSK model with Vero cells. These chemokines directly bound to HSV and the chemokine-bound HSV was later resisted by the neutralizing antibody of envelope protein gB. Furthermore, by electron microscope analysis, it became clear that these chemokines had cut an opening in the HSV envelope. Consequently, these chemokines had significantly inhibited the HSV infection on Vero cells. In addition, the virus load in tears was decreased and the corneal opacity was less severe. We concluded in that study that during early infection, chemokines accumulated in the corneal stroma have the ability to protect cells and tissues from HSV infection. As for antiviral therapy, acyclovir (ACV) eye ointment has been effective for patients with herpetic keratitis. However, patients often find it difficult to successfully follow the treatment due to the required frequent application and the blurred vision after application. On the other hand, valaciclovir (VCV), which is the oral prodrug of ACV, has become commercially available in recent years for treating nonocular herpetic diseases. We therefore examined and compared the efficacies of oral VCV, oral ACV, ACV eye ointment, and ACV eye drops in a murine keratitis model; the group treated with oral VCV did show a significantly good antiviral effect. We have proved that oral VCV can be a beneficial alternative antiviral therapy for patients with difficulty in complying with the ACV eye ointment treatment.
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PMID:[Herpes simplex virus latency, reactivation, and a new antiviral therapy for herpetic keratitis]. 1841 13

Harboyan syndrome is a degenerative corneal disorder defined as congenital hereditary endothelial dystrophy (CHED) accompanied by progressive, postlingual sensorineural hearing loss. To date, 24 cases from 11 families of various origin (Asian Indian, South American Indian, Sephardi Jewish, Brazilian Portuguese, Dutch, Gypsy, Moroccan, Dominican) have been reported. More than 50% of the reported cases have been associated with parental consanguinity. The ocular manifestations in Harboyan syndrome include diffuse bilateral corneal edema occurring with severe corneal clouding, blurred vision, visual loss and nystagmus. They are apparent at birth or within the neonatal period and are indistinguishable from those characteristic of the autosomal recessive CHED (CHED2). Hearing deficit in Harboyan is slowly progressive and typically found in patients 10-25 years old. There are no reported cases with prelinglual deafness, however, a significant hearing loss in children as young as 4 years old has been detected by audiometry, suggesting that hearing may be affected earlier, even at birth. Harboyan syndrome is caused by mutations in the SLC4A11 gene located at the CHED2 locus on chromosome 20p13-p12, indicating that CHED2 and Harboyan syndrome are allelic disorders. A total of 62 different SLC4A11 mutations have been reported in 98 families (92 CHED2 and 6 Harboyan). All reported cases have been consistent with autosomal recessive transmission. Diagnosis is based on clinical criteria, detailed ophthalmological assessment and audiometry. A molecular confirmation of the clinical diagnosis is feasible. A variety of genetic, metabolic, developmental and acquired diseases presenting with clouding of the cornea should be considered in the differential diagnosis (Peters anomaly, sclerocornea, limbal dermoids, congenital glaucoma). Audiometry must be performed to differentiate Harboyan syndrome from CHED2. Autosomal recessive types of CHED (CHED2 and Harboyan syndrome) should carefully be distinguished from the less severe autosomal dominant type CHED1. The ocular abnormalities in patients with Harboyan syndrome may be treated with topical hyperosmolar solutions. However, corneal transplantation (penetrating keratoplasty) represents definitive treatment. Corneal transplantation produces a substantial visual gain and has a relatively good surgical prognosis. Audiometric monitoring should be offered to all patients with CHED2. Hearing aids may be necessary in adolescence.
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PMID:Congenital hereditary endothelial dystrophy with progressive sensorineural deafness (Harboyan syndrome). 1892 46


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