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home:starting:physician:reluctant [08.23.2017] – [Ascertain if reluctance is a provider problem or a bureaucracy problem] sallieq | home:starting:physician:reluctant [06.01.2019] – [Specific research] sallieq | ||
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==== Ascertain if reluctance is a provider problem or a bureaucracy problem ==== | ==== Ascertain if reluctance is a provider problem or a bureaucracy problem ==== | ||
- | In Australia, physicians must now ring Canberra for permission to prescribe off-label. | + | In Australia, physicians must now approach |
- | I expect some other countries also have centralised control, in which case patients may need to research | + | < |
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+ | He simply smiled and wrote me 2 prescriptions: | ||
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+ | I expect some other countries also have centralised control, in which case patients may need to research | ||
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+ | === Specific research === | ||
[[home: | [[home: | ||
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+ | OLMesartan references to print out; for patient with doctor not a member of MPSS | ||
+ | include information about dose relating to body weight, and dose timing | ||
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+ | Dose timing -> | ||
+ | {{ : | ||
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+ | {{ : | ||
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+ | The ROADMAP study will answer the question whether an ARB can prevent or delay the onset of microalbuminuria and whether this translates into protection against cardiovascular events and renal disease. (({{pubmed> | ||
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+ | short extract for each research study follows: | ||
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+ | Benefits of RAS blockade with olmesartan treatment are sustained after study discontinued. (({{pubmed> | ||
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+ | Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects.[in rat](({{pubmed> | ||
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+ | Inhibition of renin-angiotensin system attenuates periadventitial inflammation and reduces atherosclerotic lesion formation. (({{pubmed> | ||
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+ | Olmesartan and Bay11-7082 inhibit the MCF-7 cells growth indicating RAS and NF-kappaB pathway blockade lead to cytotoxicity & apoptosis induction against tumour cells in breast cancer (({{pubmed> | ||
+ | 10) | ||
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+ | Alzheimer' | ||
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+ | prevent migraines (({{pubmed> | ||
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+ | inhibit liver fibrosis and aid liver healing (({{pubmed> | ||
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+ | 6 mg/kg olmesartan reduces the inflammatory process and bone loss [in rats] (({{pubmed> | ||
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+ | Olmesartan at a dose of 10 mg/kg prevented the mucosal damage and inflammation associated with 5-FU-induced OM, increasing granulation and tissue repair. [in hamsters] (({{pubmed> | ||
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+ | protect the mitochondria from age-associated damage from oxidation (({{pubmed> | ||
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+ | reduce liver fibrosis (({{pubmed> | ||
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+ | treatment of anxiety and stress-related disorders (({{pubmed> | ||
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+ | inflammation in myocarditis (({{pubmed> | ||
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+ | C-reactive protein, one of the acute phase proteins that increase during systemic inflammation (({{pubmed> | ||
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+ | cytokine damage (({{pubmed> | ||
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+ | in circadian rhythms between HR and MAP in CKD: Synchronization between the two rhythms was progressively lost as renal function deteriorated, | ||
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+ | renal protective effects of olmesartan may be better than those of other ARBs (({{pubmed> | ||
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+ | olmesartan may uniquely increase urinary ACE2 level, which could offer additional renoprotective effects (({{pubmed> | ||
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+ | * treatment with olmesartan inhibited bone loss (({{pubmed> | ||
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+ | * olmesartan protects endothelial cells against oxidative stress-mediated cellular injury (({{pubmed> | ||
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+ | * decreases viability of malignant cell lines(({{pubmed> | ||
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+ | * carotid IMT and BP decreased similarly with olmesartan and atenolol; but only olmesartan reduced the volume of larger atherosclerotic plaques (({{pubmed> | ||
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+ | * improvement of Plasma Biomarkers after switching stroke patients from other Angiotensin II Type I Receptor Blockers to Olmesartan (({{pubmed> | ||
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+ | * improvement of glycemic control & insulin resistance was only observed in olmesartan group (({{pubmed> | ||
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+ | * OLM substantially delayed the development of left ventricular remodeling in type 2 diabetes (({{pubmed> | ||
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+ | * prevention of microalbuminuria in patients with type 2 diabetes and hypertension (({{pubmed> | ||
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+ | Recent studies showed treatment with olmesartan inhibited bone loss (({{pubmed> | ||
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+ | olmesartan protects endothelial cells against oxidative stress-mediated cellular injury (({{pubmed> | ||
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+ | decreases viability of malignant cell lines (({{pubmed> | ||
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+ | carotid IMT and BP decreased similarly with olmesartan and atenolol; but only olmesartan reduced | ||
+ | the volume of larger atherosclerotic plaques (({{pubmed> | ||
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+ | Observations suggest a positive role in a potentially lower rate of coronary atheroma progression through the administration of olmesartan, an angiotension-II receptor blocking agent, for patients with stable angina pectoris. | ||
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+ | This study showed that olmesartan reduces angiotensin II and aldosterone levels more effectively than azilsartan. | ||
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+ | improvement of Plasma Biomarkers after switching stroke patients from other Angiotensin II Type I Receptor Blockers to Olmesartan (({{pubmed> | ||
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+ | improvement of glycemic control & insulin resistance was only observed in olmesartan group (({{pubmed> | ||
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+ | OLM substantially delayed the development of left ventricular remodeling in type 2 diabetes (({{pubmed> | ||
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+ | we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction.(({{pubmed> | ||
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+ | We orally administered olmesartan 1, 3, and 10 mg/kg/day to rats with EAM for 3 weeks. The cardioprotection of olmesartan may be due to suppression of inflammatory cytokines dependent of the hemodynamic modifications. | ||
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+ | AlphaTau1 receptor blockers, olmesartan and valsartan (10(-9)-10(-6) mol/L) showed a significant reduction on TNF-alpha-induced LDH and NAG release in human renal proximal tubular epithelial cells (({{pubmed> | ||
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+ | The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. (({{pubmed> | ||
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+ | These data added to our previous results further provide a mechanistic rationale for olmesartan' | ||
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+ | Olmesartan attenuated CTGF induction, reduced perivascular fibrosis and ameliorated cardiac dysfunction in a PO heart. Our results provide insight into the beneficial effects of olmesartan on PO hearts, independent of blood-pressure lowering. [in rat] (({{pubmed> | ||
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+ | Olmesartan treatment reversed virtually all neuroendocrine and histopathological cardiac changes induced by EAM (We used experimental autoimmune myocarditis in rats) (({{pubmed> | ||
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+ | Treatment with ARB prevents the progression of peritoneal fibrosis and suppresses expression of adhesion molecules in the peritoneum. (({{pubmed> | ||
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+ | ( in cultured human renal proximal tubular cells) Olmesartan inhibited the effect of costimulation with ANG II and IL-6 on AGT expression, indicating that AT1R is critical for AGT enhancement by ANG II. Moreover, IL-6R antibody also neutralized the effect, suggesting that these agents exert a synergistic effect, even though they do not independently induce human AGT expression. These findings suggest that AT1R blockers may attenuate the secondary pathophysiological effects of ANG II even though ANG II alone does not exert any direct effects, and this may partially account for the powerful renoprotective effects of AT1R blocker beyond its depressor effect. (({{pubmed> | ||
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+ | Olmesartan treatment had already significantly reduced serum levels of high-sensitivity C-reactive protein (-15.1%; P<0.05), high-sensitivity tumor necrosis factor-alpha (-8.9%; P<0.02), interleukin-6 (-14.0%; P<0.05), and monocyte chemotactic protein-1 (-6.5%; P<0.01) after 6 weeks of therapy, whereas placebo treatment (ie, blood pressure reduction) had no major effect on inflammation markers. (({{pubmed> | ||
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+ | Long term treatment Data suggest 40 & 80 mg olmesartan are able to significantly remodel & destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg. hyper.ahajournals.org/ | ||
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===== Read more ===== | ===== Read more ===== | ||
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{{section>: | {{section>: | ||
- | {{tag> | + | {{tag> |
===== Notes and comments ===== | ===== Notes and comments ===== |