Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sulfamethoxazole-trimethoprim (cotrimoxazole) is an antibiotic combination widely used for infections treatment and prophylaxis. These and others sulfonamides have been implicated in a rare syndrome of choroidal effusion with transient myopia and angle-closure glaucoma. Previous cases reported in literature evolved to complete resolution after drug withdrawal. In contrast, we describe a rare case in which a patient developed the syndrome while taking cotrimoxazole, but did not recover visual acuity. A 49-year-old man started Pneumocystis carini prophylaxis with cotrimoxazole; four days later, the patient presented severe ocular pain, hyperemia and chemosis. Intraocular pressure reached more than 50 mmHg in both eyes a 360 degrees choroidal effusion occurred. Medication was removed soon after the diagnosis was suspected and intraocular pressure decreased in four days. Even so total cataract and phthisis bulbi occurred in both eyes two months later. This would be the first case in the literature in which the outcome was unfavorable despite early diagnosis and withdrawal of the drug.
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PMID:[Bilateral angle-closure glaucoma induced by trimetoprim and sulfamethoxazole combination: case report]. 1776 63

While beneficial therapeutically, almost all medications have untoward effects on various body tissues and functions, including the eye in which organ toxic reactions are readily detectable. Every part of the eye and all ocular functions could be affected adversely. In this review, we describe the most commonly recognized drug-induced ocular disorders, their specific clinical features, the medications that can cause the problem, the differential diagnosis and possible mechanisms of action, as well as guidelines for the management of the adverse reactions. The eyelids are most frequently involved in drug toxicity that commonly manifests as inflammation, hypersensitivity reaction or dermatitis. Drug-induced keratoconjunctival disorders present mainly as conjunctival hyperaemia (red eye), with or without superficial corneal involvement. Frequently, drug preservatives in topical ocular medications induce these adverse effects. Treatment of blepharospasm with Botox may lead to drooping of the eyelids and corneal exposure. Intraoperative floppy iris syndrome is a drug-induced reaction in patients treated with tamsulosin and who undergo cataract surgery. Certain sulfa-based drugs can cause swelling of the ciliary body and lead to the development of angle-closure glaucoma. In addition, adrenergic agents, certain beta(2)-adrenergic agonists and anticholinergic agents may induce pupillary dilation and precipitate angle-closure glaucoma in susceptible patients. Glucocorticoids administered systemically, topically or intravitreally are known to increase intraocular pressure, which can lead to the development of open-angle glaucoma in susceptible patients. This painless form of glaucoma has also been associated with the use of the anticancer agents docetaxel and paclitaxel. The toxic effects of systemic and topically applied drugs may manifest as cloudiness of the lens. Long-term use of glucocorticoids produces a characteristic posterior subcapsular cataract and, although the opacities may remain stationary or progress, they rarely regress upon drug withdrawal. Systemic administration of phenothiazines or busulfan induce cataractous changes in the anterior or posterior cortex, respectively. Many systemic drugs reach the retina through the vascular supply. Aminoquinolines induce a characteristic bull's eye maculopathy. Phenothiazines bind to melanin granules and can cause a severe phototoxic retinopathy. Typical tamoxifen retinopathy manifests as crystalline deposits in the inner retina. Some patients treated with retinoids have decreased night vision and abnormal dark-adaptation. Patients on long-term treatment with linezolid may develop an optic neuropathy (swollen or pale optic disc), symmetric painless decrease of visual acuity and colour vision, and bilateral visual field defects. A probable link exists between amiodarone and a bilateral optic neuropathy that is very similar to nonarteritic ischaemic optic neuropathy (NAION). The most common adverse effects of cGMP-specific phosphodiesterase type 5 inhibitors (erectile dysfunction drugs) are changes in colour perception, blurry vision and increased light sensitivity; recently these drugs have been also implicated in the development of NAION. A bilateral, retrobulbar optic neuropathy that manifests as loss of visual acuity or colour vision and visual field defect is associated with the use of ethambutol. Many different kinds of medications can cause similar ocular adverse reactions. Conversely, a single medication may affect more than one ocular structure and cause multiple, clinically recognizable disorders. Clinicians should be mindful of drug-induced ocular disorders, whether or not listed in product package inserts, and, if in doubt, consult with an ophthalmologist.
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PMID:Drug-induced ocular disorders. 1821 89

When corticosteroid therapy, immunoglobulin and splenectomy fail to control chronic idiopathic thrombocytopenic purpura and the risk of bleeding remains high, romiplostim is an acceptable option but close monitoring is needed to evaluate long-term risks. Eltrombopag (Revolade, GlaxoSmithKline) is a synthetic non-peptide agonist of endogenous receptors for thrombopoietin, a platelet growth factor. Clinical evaluation of eltrombopag in this setting is mainly based on a double-blind placebo-controlled trial in a heterogeneous group of 114 patients. The platelet count rose to at least 50,000/mm3 for five weeks in about one-quarter of patients receiving oral eltrombopag 50 mg/day. An indirect comparison providing weak evidence suggests that romiplostim is more effective. Clinical trials did not provide evidence that either drug reduced the frequency of bleeding. The haematological risks associated with eltrombopag are poorly evaluated, and mainly include: thrombosis, bone marrow disorders, and aggravation of thrombocytopenia after drug withdrawal. Aggravation of myelodysplastic syndrome cannot be ruled out in the long term. Hepatic disorders such as photosensitisation are frequent. The risk of cataract formation and renal impairment requires further study. There appears to be a high risk of pharmacokinetic interactions through a variety of mechanisms, including enzyme competition and cation binding, but this risk is not well documented. Eltrombopag is administered orally, making it more convenient than romiplostim, which necessitates weekly subcutaneous injections. In practice, when standard treatments fail in patients with chronic idiopathic thrombocytopenic purpura and a high risk of bleeding, it is better to use romiplostim, which appears to be somewhat more effective than eltrombopag. Eltrombopag also seems to carry a higher risk of non-haematological adverse effects and drug interactions.
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PMID:Eltrombopag. Idiopathic thrombocytopenic purpura after treatment failure: romiplostim is a better option. 2045 33