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)

Diabetes is known to be associated with an increase in aldose reductase activity, platelet hyperaggregability, lipid peroxidation, and cataract formation. A molecule, D-myo-inositol 1,2,6-trisphosphate (PP-56), derived from phytic acid, could in principle, by supplying myoinositol to tissues and acting as an antioxidant, counteract some of the manifestations of diabetes. Thus, the effects of PP-56 on platelet aggregation, fatty acids, and polyols were investigated in uncontrolled streptozotocin-induced diabetes in rat in relation to cataract and lipid peroxidation. A decrease in the response of platelet aggregation to thrombin and ADP (P less than 0.05, P less than 0.001) and in the level of sorbitol and the ratio sorbitol/myo-inositol (P less than 0.01) in platelets was observed in the rats treated by PP-56 for 7-8 weeks. These beneficial effects were associated with an incidence of cataract reduced by 26 to 44% (P less than 0.05 to P less than 0.001) depending on the duration of treatment. They were also accompanied by a significant lower plasma level of malondialdehyde (P less than 0.05), and, more markedly, of conjugated dienes (P less than 0.001) as well as an increase in platelet lipids of the 20:4(n-6)/20:3(n-6) ratio, an index of delta 5 desaturase activity. PP-56 appears to modulate fatty acid desaturases and aldose reductase in platelets and delay by a few weeks the development of cataract in this acute model of diabetes.
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PMID:Effect of D-myo-inositol on platelet function and composition and on cataract development in streptozotocin-induced diabetic rats. 138 35

We report the case of a patient with recurrent hemorrhagic choroidal detachments after combined cataract and filtering surgery associated with exacerbation of chronic disseminated intravascular coagulation (DIC). It was postulated that the formation and drainage of the hemorrhagic choroidal detachments induced thrombin generation and consequently coagulation factor and platelet consumption. Fibrinolysis resulted in the release of fibrin-degradation products (FDP). Consumption of clotting factors and platelets combined with FDP release may result in decompensation of a chronic DIC state and cause a bleeding diathesis. This case shows the need for complete hematologic evaluation of patients with hemostatic abnormalities.
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PMID:Recurrent hemorrhagic choroidal detachment associated with disseminated intravascular coagulation. 156 29

Cryoprecipitate and thrombin were used to prevent bleeding and induce permanent conjunctival attachment in ten cases of retinal detachment, 40 cases of extracapsular cataract extraction, and ten cases of strabismus. This method proved to be a good alternative to suturing the conjunctiva in each of the above-mentioned surgical procedures, and appears to result in a better and more comfortable postoperative course.
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PMID:Use of fibrin glue in ocular surgery. 334 59

A series of coagulation parameters and lipoprotein(a) (Lp(a)) were explored in plasma from 40 patients with central retinal vein occlusion (CRVO, non-ischemic type n = 12; ischemic type n = 28) free of local and systemic predisposing factors, 1 to 12 months after the acute event. Forty age- and sex-matched patients with cataract served as controls. Prothrombin fragment 1.2 (F1.2), D-dimer, FVII:C--but not FVII:Ag--were higher and fibrinogen was lower in CRVO patients than in controls. Patients with non-ischemic CRVO had higher F1.2 and FVII:C and lower heparin cofactor II than patients with ischemic CRVO. Lp(a) levels greater than 300 mg/l were observed in 12 patients with CRVO and in 4 controls (30% vs 10%, p < 0.025). Patients with high Lp(a)--consistently associated with the S2 phenotype--had higher FVII:C, FVII:C/Ag ratio, and fibrinogen than the remaining CRVO patients. Plasma F1.2 and D-dimer correlated fairly in controls (r = 0.41) and patients with normal Lp(a) levels (r = 0.55), but they did not in the group of patients with high Lp(a) (r = 0.19), where the latter parameter was negatively related to D-dimer (r = -0.55). There was no dependence of the abnormalities observed on the time elapsed from vein occlusion. The findings of activated FVII and high F1.2, D-dimer, and Lp(a) are not uncommon in patients with CRVO. Increased thrombin formation with fibrin deposition and impaired fibrinolysis may play a role in the pathophysiology of CRVO and require specific treatment.
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PMID:Hypercoagulability and high lipoprotein(a) levels in patients with central retinal vein occlusion. 797 73

Oxidative processes in the lenses are the most commonly found damaging factor for the development of cataracts. Hirudin, a most potent inhibitor of thrombin as an antithrombic drug, also have potential use in cataracts. In order to investigate the mechanisms of hirudin against galactose-induced cataract at the cellular level. We used recombinant hirudin variant III (rHV3) to study the protective effect of hirudin on galactose-mediated human lens epithelial cells injury. The human lens epithelial cells (hLECs) were cultured in D/F(12)-10% FBS medium containing 125 mM D-galactose with or without rHV3. Cell viability was assessed by methylthiazol tetrazolium (MTT) assay and propidium iodide (PI) staining in situ. Cell apoptosis was elevated with comet assay (single cell gel electrophoresis, SCGE), AO/EB double staining and Annexin-V/PI double staining assay. Reactive oxygen species (ROS) were quantified with 2',7'-dichlorofluorescein (DCF), and free glutathione (GSH) levels were measured with a commercial GSH quantification kit. Decreased viability and increased apoptosis of the hLECs were observed when incubated with 125 mM galactose. These hLECs also demonstrated the increased presence of ROS, whereas GSH was reduced. rHV3 blocked the induction of cell death, apoptosis and oxidative stress in hLECs. One mechanism may be through regulating intracellular ROS and GSH levels to inhibit apoptosis of the human lens epithelial cells.
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PMID:Intracellular GSH and ROS levels may be related to galactose-mediated human lens epithelial cell apoptosis: role of recombinant hirudin variant III. 1902 24

MYH9-related platelet disorders are inherited macrothrombocytopenias with additional clinical manifestations including renal failure, hearing loss, pre-senile cataract, and inclusion bodies in leucocytes that are present in different combinations. The MYH9 gene codes for the cytoplasmic contractile protein non-muscular myosin heavy chain IIA, present in several tissues. The bleeding tendency is usually mild to moderate but rarely, thrombotic complications are also seen. We report on the thrombin generation potential (ETP) in patients with MYH9-related disease with and without arterial thrombosis. In family A, four affected members [c.5521G>A mutation causing p.(Glu1841Lys)] were evaluated. Three of them had a moderate bleeding tendency and in two renal insufficiency and hearing loss were already present. These two patients had an arterial thrombosis (myocardial infarction and pons infarction, respectively) before 50 years of age. In family B, two members were affected [c.4679T>G, resulting in p.(Val1560Gly)]. Their bleeding tendency was mild (bleeding scores 4 and 3, respectively). Thrombelastography (ROTEM) was normal in all six individuals. ETP was below the normal range in family B. However, in family A, the two members affected by thrombosis had a normal ETP, indicating that other factors compensated for the low platelet count and might have contributed to the arterial thrombosis.
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PMID:Thrombin generation in two families with MYH9-related platelet disorder. 2624 37