Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prognosis of some of the most prevalent conditions seems to be intricately related to myriad risk factors, largely modifiable, but often leading to irreversible complications when left unmanaged. This study exemplifies the multidisciplinary approach necessary, to successfully control diabetic retinopathy, one of the leading complications of diabetes, and to discuss promising therapies. Based on a Medline Ovid database search, we present a clinical and economic review of the evidence on the epidemiology and risk factors of diabetic retinopathy, its prognosis and economic implications. Among adults aged 20-74, diabetic retinopathy (DR) is the most frequent cause of blindness. However, in both types 1 and 2 DM, improved glycemic control reduces the development and progression of DR. Risk factors of DR include duration of diabetes, pregnancy, renal disease, age, smoking, alcohol, hyperlipidemia and antioxidants. A number of drugs may play a role in DR therapy in the coming few years; eg, somatostatin agonists (sandostatin), corticosteroids (triamcinolone, dexamethasone, fluocinolone), vascular endothelial growth factor inhibitors (pegaptanib, ranibizumab), hyaluronidase and plasmin enzyme. Whether these therapies have a clinically significant impact on DR progression however, remains to be seen.
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PMID:Diabetic retinopathy. 1966 79

The endothelial glycocalyx has a profound influence at the vascular wall on the transmission of shear stress, on the maintenance of a selective permeability barrier and a low hydraulic conductivity, and on attenuating firm adhesion of blood leukocytes and platelets. Major constituents of the glycocalyx, including syndecans, heparan sulphates and hyaluronan, are shed from the endothelial surface under various acute and chronic clinical conditions, the best characterized being ischaemia and hypoxia, sepsis and inflammation, atherosclerosis, diabetes, renal disease and haemorrhagic viral infections. Damage has also been detected by in vivo microscopic techniques. Matrix metalloproteases may shed syndecans and heparanase, released from activated mast cells, cleaves heparan sulphates from core proteins. According to new data, not only hyaluronidase but also the serine proteases thrombin, elastase, proteinase 3 and plasminogen, as well as cathepsin B lead to loss of hyaluronan from the endothelial surface layer, suggesting a wide array of potentially destructive conditions. Appropriately, pharmacological agents such as inhibitors of inflammation, antithrombin and inhibitors of metalloproteases display potential to attenuate shedding of the glycocalyx in various experimental models. Also, plasma components, especially albumin, stabilize the glycocalyx and contribute to the endothelial surface layer. Though symptoms of the above listed diseases and conditions correlate with sequelae expected from disturbance of the endothelial glycocalyx (oedema, inflammation, leukocyte and platelet adhesion, low reflow), therapeutic studies to prove a causal connection have yet to be designed. With respect to studies on humans, some clinical evidence exists for benefits from application of sulodexide, a preparation delivering precursors of the glycocalyx constituent heparan sulphate. At present, the simplest option for protecting the glycocalyx seems to be to ensure an adequate level of albumin. However, also in this case, definite proof of causality needs to be delivered.
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PMID:Degradation of the endothelial glycocalyx in clinical settings: searching for the sheddases. 2577 76