Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old woman has been suffering from recurrent corneal edema without ocular hypertension since her early childhood. When the cornea is clear, visual acuity-with correction for high myopia-is 5/10 to 5/15 and Nieden I; when the cornea is swollen, it decrease to 5/50 and 1/10, respectively, and Nieden VII. Furthermore, there is an atypical pigment degeneration of the retina combined with deafness, a progressive ptosis since her 10th year of life, and a progressive dystrophy of the outer eye muscles, having developed in the past few years. In addition, the mentally normal developed patient presents a proportional dwarfism (no dysostosis) and a diabetes mellitus. This combination of symptoms is compared with the well known Bardet-Biedl syndrome and the De Grouchy syndrome and is found to constitute a new syndrome.
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PMID:[Recurrent corneal edema without ocular hypertension, pigment degeneration combined with deafness, progressive dystrophy of the outer eye-muscles in a patient with proportional dwarfism and diabetes mellitus (author's transl)]. 30 14

A trial of a mixture of guanethidine 5% and adrenaline 0.5% (Ganda 5.05) and of guanethidine 3% and adrenaline 0.5% (Ganda 3.05) was conducted on 90 eyes in 53 patients with open-angle glaucoma or ocular hypertension. The cases fell into 5 groups: untreated cases, cases on pilocarpine 1%, on pilocarpine 2%, on pilocarpine 2 to 4% and adrenaline 1%, and on separate guanethidine 5% and adrenaline 1%. Baseline pressures and average pressures on the previous treatment were established. Substitution with Ganda 3.05 or 5.05 was started, and the patients attended 2 weeks, 1 month, 3 months, and 6 months from the start of the trial. Applanation tonometry was carried out at the same time of day. The pupil was measured, ptosis and superficial punctate corneal staining were looked for and evaluated, and the patients were questioned for symptoms of side effects and acceptability. All the eyes that had previously been treated with pilocarpine 1% or 2% presented significantly lower intraocular pressures on Ganda 3.05. The patients on pilocarpine 4% and adrenaline 1% also had lower intraocular pressures on Ganda 5.05, but the significance was less, and the patients on separate guanethidine and adrenaline had a small but not statistically significant drop in pressure. Ptosis and discomfort were evaluated on a subjective scale. Patient acceptability was good. The trial was interrupted in 5 cases for various reasons. Tachyphylaxis and tolerance to the mixtures were not observed in this series.
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PMID:Evaluation of a 5% guanethidine and 0.5% adrenaline mixture (Ganda 5.05) and of a 3% guanethidine and 0.5% adrenaline mixture (Ganda 3.05) in the treatment of open-angle glaucoma. 36 32

Herpes zoster ophthalmicus was seen in 22 cases out of 195 cases of herpes zoster (11.3% incidence). It was affecting mainly adults (90.9%). Oedema over the lids (81.8%) was invariably present and lead to ptosis. Mucopurulent conjunctivitis, predominantly mucoid (72.7%) was the commonest manifestation associated with vesicles over the lid margins. Sectorial (22.7%) and diffuse (9.1%) episcleritis appeared in later part of first week, while nodular episcleritis was observed in one case only on 12th day of the disease. Nummular keratitis was seen in 31.8% of cases between 8-10 days. Iritis and iridocyclitis was seen in 45.4% of cases out of which 36.3% had secondary ocular hypertension (glaucoma). Neuroparalytic keratitis and internal ophthalmoplegia were detected in one patient each. Postherpetic neuralgia occurred in 22.7% of cases and was uncommon in younger age group (below 40 years, 4.5%). Carbamazepine was effective in relieving the herpetic pain.
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PMID:Clinical profile of herpes zoster ophthalmicus. 174 74

Corticosteroids, used prudently, are one of the most potent and effective modalities available in the treatment of ocular inflammation. However, they can produce a plethora of adverse ocular and systemic events. In order to optimise and target drug delivery, whilst minimising systemic adverse effects, a diverse range of local ophthalmic preparations and delivery techniques have been developed. Topical drops and ointments remain the primary methods for administration of ocular corticosteroids. However, ocular penetration of topical corticosteroid drops depends upon drug concentration, chemical formulation of corticosteroid, and composition of the vehicle, therefore, apparently small modifications in preparations can produce a more than 20-fold difference in intraocular drug concentration. Periocular injections of corticosteroids continue to have a useful, but limited, therapeutic role and longer acting, intraocular delayed-release devices are in early clinical studies. Although newer corticosteroids with lesser pressure elevating characteristics have been developed, corticosteroid-induced ocular hypertension and glaucoma continue to be significant risks of local and systemic administration. Posterior subcapsular cataract, observed following as little as 4 months topical corticosteroids use, is thought to be due to covalent binding of corticosteroid to lens protein with subsequent oxidation. Inappropriate use of topical corticosteroid in the presence of corneal infections also continues to be a cause of ocular morbidity. Other risks of locally administered ophthalmic corticosteroids include: tear-film instability, epithelial toxicity, crystalline keratopathy, decreased wound strength, orbital fat atrophy, ptosis, limitation of ocular movement, inadvertent intraocular injection, and reduction in endogenous cortisol. This extensive review assesses the therapeutic benefits of locally administered ocular corticosteroids in the context of the risks of adverse effects.
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PMID:Locally administered ocular corticosteroids: benefits and risks. 1182 Sep 11

An eight-year-old female spayed Boston Terrier presented to the North Carolina Veterinary Hospital with glaucoma in the left eye (OS). Initial ophthalmic examination revealed moderate ocular hypertension, a diffusely and markedly shallow anterior chamber with anteriorly displaced iris and lens, vitreal prolapse, and a normal iridocorneal angle (ICA) morphology. The patient displayed a paradoxical response to topical latanoprost with an increase in intraocular pressure. These examination findings led to a putative diagnosis of spontaneous aqueous humor misdirection syndrome (AHMS). The patient was successfully managed with topical carbonic anhydrase inhibitors (CAIs) and apraclonidine for eight months until progressive ulcerative keratitis necessitated enucleation of the affected globe. Histopathology and high-field magnetic resonance imaging (MRI) of the enucleated globe did not identify an underlying cause for the glaucoma. This case suggests that AHMS should be considered in dogs presenting with a shallow anterior chamber, vitreal prolapse, increased intraocular pressure, and no other causes of glaucoma.
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PMID:Suspected Spontaneous Aqueous Humor Misdirection Syndrome in a Boston Terrier. 3255 38