Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin analogues are a therapeutic option in patients with chronic overproduction of growth hormone (GH) and insulin-like growth factor 1 (IGF-1). These factors are also involved in the pathogenesis of diabetic retinopathy. Somatostatin receptors are expressed in the retina and are therefore possible targets of somatostatin analogues in the treatment of retinal vascular diseases like diabetic retinopathy. The somatostatin analogue octreotide has shown promise as a safe and effective treatment for advanced diabetic retinopathy and diabetic macular edema. The compound blocks the local and systemic production of GH and IGF-1, and thus inhibits the angiogenic effect. Evidence from animal models, and clinical trials in patients with diabetic retinopathy, suggest that octreotide can delay, and to some extent reverse diabetic retinopathy.
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PMID:[Therapy of diabetic retinopathy with somatostatin analogues]. 1500 9

Chronic overproduction of growth hormone and insulin-like growth factor 1 play an important role in the pathogenesis of diabetic retinopathy. Somatostatin receptors are the targets of somatostatin analogues such as octreotide in the treatment of diabetic retinopathy. Octreotide has shown promise as a safe and effective treatment for advanced diabetic retinopathy and diabetic macular edema. One important pathomechanism in the development of diabetic complications is the activation of protein kinase C induced by high glucose due to an increased diacylglycerol level. The development of a selective PKCss inhibitor enables a new therapeutic approach for the treatment of diabetic retinopathy. Ongoing prospective clinical studies are investigating if treatment with specific PKCss inhibitors can prevent the progression of diabetic retinopathy and diabetic macular edema. The intravitreal injection of triamcinolone acetonide leads to at least temporary improvement of the diffuse diabetic macular edema. Side effects are increase of intraocular pressure, cataract, and endophthalmitis.
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PMID:[Pharmacological treatment of diabetic retinopathy]. 1559 46

Despite the better options of controlling diabetes mellitus and although the prognosis of diabetic retinopathy has markedly improved by laser treatment and vitreoretinal surgery, diabetic retinopathy still is the leading cause of blindness in working age people in industrialized countries. Little has changed in the last decades regarding the prognosis of ocular complications in diabetes mellitus. We therefore need better tools and new therapeutic approaches for the prevention and treatment of diabetic ocular complications. Newer therapeutic options are directed at the causative mechanisms of diabetic retinopathy. Experimental and clinical evidence suggests that pharmacological compounds like somatostatin analogues and protein kinase C (PKC) inhibitors may be effective in the treatment of diabetic retinopathy. Chronic overproduction of growth hormone and insulin-like growth factor 1 play an important role in the pathogenesis of diabetic retinopathy. In the treatment of diabetic retinopathy somatostatin receptors are the targets of somatostatin analogues like octreotide. Octreotide has shown to be a promising treatment of diabetic retinopathy and diabetic macular edema. One important pathomechanism in the development of diabetic retinopathy is the activation of PKC induced by high glucose due to an increased diacylglycerol level. The selective PKC-beta inhibitor ruboxistaurin mesylate enables a new therapeutical approach for the treatment of diabetic retinopathy. Ongoing prospective clinical trials investigate whether the treatment with the specific PKC-beta inhibitor can prevent the progression of diabetic retinopathy and diabetic macular edema.
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PMID:Pharmacological treatment of diabetic retinopathy. 1738 65

Diabetic retinopathy continues to be the leading cause of legal blindness among working-age individuals. The earliest histological features of diabetic retinopathy include neuroretinal damage, capillary basement membrane thickening, loss of pericytes and loss of endothelial cells. At advanced stages, neovascularization, the hallmark of proliferative diabetic retinopathy (PDR) occurs, and blindness can result from relentless abnormal fibrovascular proliferation with subsequent bleeding and retinal detachment. Macular oedema is another retinal complication of diabetes that is responsible for a major part of vision loss, particularly in type 2 diabetes. The breakdown of the blood retinal barrier and the consequent vascular leakage and thickening of retina are the main events involved in its pathogenesis. Although a tight control of both blood glucose levels and hypertension are essential to prevent or arrest progression of the disease, the recommended goals are difficult to achieve in many patients. Laser photocoagulation treatment soon after the onset of PDR significantly reduces the incidence of severe vision loss. However, the optimal timing for laser treatment is frequently passed and, in addition, it is not uniformly successful in halting visual decline. For all these reasons, new pharmacological treatments based on the understanding of the pathophysiological mechanisms of diabetic retinopathy have been developed in recent years. There is mounting evidence to suggest that angiogenic factors play a crucial role in PDR development, vascular endothelial growth factor (VEGF) being the most relevant. Other growth factors or cytokines such as insulin-like growth factor I (IGF-1), hepatocyte growth factor (HGF), basic fibroblast growth factor (b-FGF), platelet derived growth factor (PDGF), pro-inflammatory cytokines and angiopoetins, are also involved in the pathogenesis of PDR. However, the intraocular synthesis of angiogenic factors is counterbalanced by the synthesis of antiangiogenic factors. Therefore, the balance between the angiogenic and antiangiogenic factors rather than angiogenic factors themselves will be crucial in determining the progression of PDR. The main antiangiogenic factor is the pigment epithelium derived factor (PEDF) but the transforming growth factor beta (TGF-beta), thrombospondin (TSP) and somatostatin are also among the intraocullary synthesized antiangiogenic factors.
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PMID:Angiogenic and antiangiogenic factors in proliferative diabetic retinopathy. 1822 Jun 19

Diabetic macular edema is one of the leading causes of visual loss in first world countries and the first cause in diabetic retinopathy. The Early Treatment Diabetic Retinopathy Study showed a significant benefit in using focal laser photocoagulation for the treatment of macular edema, more specifically defined as clinically significant macular edema. Nevertheless, progressive visual loss is found in the 26% of patients with diabetic macular edema treated with photocoagulation. The failure of laser treatment and the destructive nature of the therapy has forced researchers to pursue new alternatives including vitrectomy with or without internal limiting membrane peels, the use of proteinkinase C inhibitors, intravitreal injections of antibodies that inhibit the vascular endothelial growth factor, somatostatin analog, or the intravitreal injection with corticosteroids. Triamcinolone acetonide is glucocoticosteroid with antiangiogenic and antiedematous properties. Publications evaluating the safety and efficacy of intravitreal injection of triamcinolone in the treatment of diabetic macular edema show varying outcomes with respect to the increases of visual acuity and decreases in foveal thickness. Despite this, intravitreal triamcinolone is a treatment that has evolved quickly and is considered increasingly useful.
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PMID:Intravitreal triamcinolone for the treatment of diabetic macular edema. 1822 Jun 20

Somatostatin analogs are an invaluable therapeutic option in the diagnosis and treatment of somatotropinomas, thyrotropinomas, and functioning and non-functioning gastroenteropancreatic neuroendocrine tumors. They should also be considered an effective and safe therapeutic alternative to corticotropinomas, gonadotropinomas, and prolactinomas resistant to dopamine agonists. Somatostatin analogs have also shown to be useful in the treatment of other endocrine diseases (congenital hyperinsulinism, Graves' orbitopathy, diabetic retinopathy, diabetic macular edema), non-endocrine tumors (breast, colon, prostate, lung, and hepatocellular), and digestive diseases (chronic refractory diarrhea, hepatorenal polycystosis, gastrointestinal hemorrhage, dumping syndrome, and intestinal fistula).
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PMID:Somatostatin Analogs in Clinical Practice: a Review. 3212 32