Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Schnyder corneal dystrophy (SCD) is a rare corneal dystrophy characterized by abnormally increased deposition of cholesterol and phospholipids in the cornea leading to progressive vision loss. SCD is inherited as an autosomal dominant trait with high penetrance and has been mapped to the UBIAD1 gene on chromosome 1p36.3. Although 2/3 of SCD patients also have systemic hypercholesterolemia, the incidence of hypercholesterolemia is also increased in unaffected members of SCD pedigrees. Consequently, SCD is thought to result from a local metabolic defect in the cornea. The corneal findings in SCD are very predictable depending on the age of the individual, with initial central corneal haze and/or crystals, subsequent appearance of arcus lipoides in the third decade and formation of midperipheral haze in the late fourth decade. Because only 50% of affected patients have corneal crystals, the International Committee for Classification of Corneal Dystrophies recently changed the original name of this dystrophy from Schnyder crystalline corneal dystrophy to Schnyder corneal dystrophy. Diagnosis of affected individuals without crystalline deposits is often delayed and these individuals are frequently misdiagnosed. The differential diagnosis of the SCD patient includes other diseases with crystalline deposits such as cystinosis, tyrosinemia, Bietti crystalline dystrophy, hyperuricemia/gout, multiple myeloma, monoclonal gammopathy, infectious crystalline keratopathy, and Dieffenbachia keratitis. Depositions from drugs such as gold in chrysiasis, chlorpromazine, chloroquine, and clofazamine can also result in corneal deposits and are different from SCD. Diseases of systemic lipid metabolism that cause corneal opacification, such as lecithin-cholesterol acyltransferase deficiency, fish eye disease and Tangier disease, should also be considered although these are autosomal recessive disorders.
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PMID:Differential diagnosis of Schnyder corneal dystrophy. 2154 Jun 32

This study evaluated the effect of gout on the risk of dry eye disease (DED) by using the National Health Insurance Research Database (NHIRD). Data for 30,192 gout patients (21,081 men and 9111 women) and 30,192 non-gout patients (21,005 men and 9187 women) were analyzed. Approximately 1 million patients were randomly sampled from the NHIRD registry. After applying exclusion criteria, patients diagnosed with gout were enrolled in the study group. Thereafter, each individual in the study group underwent the matching process via the propensity score with another non-gout individual, which constituted the control group. The main outcome was defined as the development of DED in accordance with the corresponding International Classification of Diseases, Ninth Revision. In addition to DED, other risk factors including age, sex, and urbanization, and several co-morbidities were included in the multivariate model. The incidence of DED with the adjusted hazard ratio (aHR) and cumulative probability were evaluated in the gout and non-gout patients. A total of 2913 DED events were observed in the study group, whereas 2631 DED events were observed in the control group. A higher incidence rate ratio was found in the study group after adjustment (aHR: 1.065). Moreover, the cumulative probability indicated a significantly increased risk of DED in the study group (p = 0.001). The other potential risk factors of DED according to the multivariate analysis include older age, female gender, higher degree of urbanization, keratopathy, age-related macular degeneration, glaucoma, cataract, ischemic heart disease, hyperlipidemia, peripheral vascular disease, chronic pulmonary disease, rheumatic disease, peptic ulcer disease, liver disease, and malignancy. In conclusion, gout increased the risk of DED after adjustment, and the risk is positively correlated to a longer disease period.
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PMID:Gout as a Risk Factor for Dry Eye Disease: A Population-Based Cohort Study. 3063 89

We present the management of three cases of infectious crystalline keratopathy. The first one, in a 46-year-old patient with two previous penetrating keratoplasties; the second one, in a 46-year-old patient with chronic alcoholism and limbal insufficiency; and the third one, in a 70-year-old patient with bullous keratopathy. Other systemic conditions that may mimic infectious crystalline keratopathy, such as multiple myeloma, gout or cystinosis were ruled out on each patient by laboratory testing. The cases were managed with topical or topical and systemic treatment that led to the disappearance of the symptoms. Infectious crystalline keratopathy is a chronic and indolent pathology in which interlamellar bacterial plaques are observed in absence of apparent ocular inflammatory signs. Microorganisms penetrate the cornea through epithelial defects, commonly after a penetrating keratoplasty, although other risk factors may be present.
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PMID:Infectious crystalline keratopathy: Management of three cases with different risk factors. 3192 Apr 55