Tuesday, July 15, 2008

BBC SPORT | Cricket | England | India hold nerve to level series

low back pain treatment Second one-day international, Bristol:
India 329-7 (50 ovs) bt England 320-9 (50 ovs) by nine runs

India beat England by nine runs to level the one-day international series.

Sachin Tendulkar struck 15 fours and a six in an epic 99, his 80th ODI fifty and Rahul Dravid hit an unbeaten 92 as India scored 329-7 after opting to bat.

England raced to 76 within 11 overs but lost both openers in two balls. Piyush Chawla ousted Kevin Pietersen with his second ball but Ian Bell hit a calm 64.

Dimitri Mascarenhas fired five sixes in 52 off 39 balls and Stuart Broad hit 20 in the last over in a frantic finale.

Interview: England one-day captain Paul Collingwood Interview: India captain Rahul Dravid

After the arctic conditions at the Rose Bowl on Tuesday evening, the weather was much more to the liking of the Indian team and their many followers.

While the tourists added another spinner to their ranks in Ramesh Powar, England omitted Monty Panesar and picked another seamer, Chris Tremlett.

Dravid had little hesitation in batting first and it quickly became apparent there was little assistance in the pitch for the bowlers.

For a brief period the attacking shots found the fielders but it did not last and Tendulkar began to play in virtuoso fashion, finding the gaps to the small boundaries.

Paul Collingwood elected to take the final powerplay but Ganguly launched Tremlett back over his head for six in an over costing 17.

Tremlett also spilled a tough chance when Tendulkar was on 57, but was perhaps the only man tall enough to have got his hands to a rasping aerial drive.

The next ball produced a wicket, Collingwood taking an excellent catch running backwards at point when Ganguly carved a drive.

Tremlett returned and was promptly despatched for another six, Tendulkar stepping down the pitch to fizz the ball over long-off.

The only obstacle to Tendulkar reaching three figures appeared to be injury and the maestro received lengthy treatment to his hands, wincing at the sharp pain.

He had another reprieve on 93 when he glanced Collingwood but Matt Prior could not hold a sharp chance down the leg-side.

But when Tendulkar was on 99 Andrew Flintoff produced a magnificent bouncer that reared up from the unresponsive pitch and surprised the icon, who fended the ball away.

Prior leapt superbly to snare the catch diving to his left and Tendulkar was denied a 42nd ODI century, much to the dismay of his adoring fans.

Another neat Collingwood catch, this time low at point, accounted for Yuvraj Singh for 49, but that merely allowed Mahendra Dhoni the chance to cut loose in nine overs.

Dravid reached fifty from 43 balls and was the dominant partner in a stand of 59 from 38 deliveries to which Dhoni contributed 21.

Tremlett, moved to backward square-leg after some lax fielding on the boundary improved his wretched day somewhat when he took a fine catch when Dhoni paddled a slower ball.

Even more worrying news for England was a scare to Flintoff, who crashed into the advertising boards in pursuit of the ball and suffered pain behind his knee.

There was still time for more fireworks, Dravid firing a square drive off Anderson for six and guiding a late cut for four, Flintoff with two wickets in the final over to take his first one-day five-wicket haul.

Because of the length of time taken to bowl the overs, there were barely 10 minutes between innings, but although the floodlights were on there was bright sunshine when England began their quest for a record total.

It was an electrifying start, Alastair Cook and Prior with some fluent strokes, Ajit Agarkar conceding 41 from his first four overs.

Prior was caught off a no-ball but two balls later drove wildly at Munaf Patel and Dravid held a spiralling chance at mid-off.

The batsmen crossed and Patel produced a good one next up to take Cook's edge.

In the next over Bell, on one, played an upper cut straight to third man but the portly Powar spilled the chance.

Still the chances came - and went. In Ganguly's first over, Dhoni juggled with a routine Pietersen edge at the stumps and the bowler himself then failed to take a low return catch.

But teenage leg-spinner Chawla made another key breakthrough, squeezing his second delivery between an incredulous Pietersen's bat and pad.

Chawla and Powar then bowled in tandem, with clever variations, and the rate slipped over seven, Collingwood having made a typically enterprising 27 deceived by Chawla's googly.

Flintoff started in superb fashion, thumping his first ball through the covers and pulling his third delivery for another lusty boundary.

But once again he picked out a fielder with a lofted stroke, Agarkar not having to move at deep mid-wicket.

Ravi Bopara added 35 in seven overs with Bell in calm fashion but when he was plumb lbw to Patel, 110 were still needed from 73 balls and only four wickets remained.

As he demonstrated in his century at the Rose Bowl, Bell danced down the wicket to hit an imperious first six, but attempting to repeat the stroke next ball he could not connect with the middle of the bat and the stroke went straight to Patel on the long-on fence.

Mascarenhas hit the spinners for three sixes to reduce the requirement to 65 from the final six overs and added two more, sending one shot into the guttering of the stand, before mis-cueing to mid-wicket in the penultimate over.

Patel bowled the final over with the cushion of 30 to play with.

Left-hander Broad swung the first ball to mid-wicket where Powar took the ball over the ropes, and two bottom edges for four plus another maximum left 10 needed from the final ball and Patel ensured he did not over-step.

This is a part of article BBC SPORT | Cricket | England | India hold nerve to level series Taken from "Generic Arcoxia (Etoricoxib)" Information Blog

Thursday, July 10, 2008

‘The drugs are worth the risk’

arcoxia A large UK study has found that painkillers used for the treatment of arthritis - COX-2 inhibitors such as arcoxia and other such as ibuprofen and diclofenac - increase the risk of heart attack.

But many patients are completely dependent on the drugs to control their pain, and feel the risk is worth taking.

Catherine Cribb tells the BBC what it's like to live with arthritis.

"I have had rheumatoid arthritis for 15 years.

"I'm currently taking arcoxia which makes life worth living."

"Without it, I wouldn't be able to get moving in the morning.

"I have seen people taken off the drugs and put on paracetamol and they are really struggling - it doesn't even touch the pain."

'Unbearable pain'

Catherine, aged 58, lives in Formby, Merseyside, and has tried many drugs over the years to help control her condition, including ibuprofen, and believes the increased risk of heart attack is nothing compared to the quality of life she gets from the drugs.

"The best ones for me are the COX-2s but it doesn't suit everybody.

"People have to work out what's best for them.

"I don't think people realise how bad it is - sometimes I won't want to stand up because I know the pain will be unbearable.

"There's risks to everything but without these drugs there would be no point carrying on," she said.

"You have to be able to live life."
This is a part of article ‘The drugs are worth the risk’ Taken from "Generic Arcoxia (Etoricoxib)" Information Blog

Saturday, July 05, 2008

Combination Therapy: The Future of Medical Management for PAH


Rationale for Combining Therapies

The current treatment strategy for PAH targets the mediators of the 3 main biologic pathways that are critical to its pathogenesis and progression (Figure 3). Endothelin receptor antagonists inhibit the activated endothelin pathway by blocking the biologic activity of the mediator endothelin-1, phosphodiesterase-5 (PDE-5) inhibitors increase endogenous availability of cyclic guanosine monophosphate (cGMP), which signals the vasorelaxing effects of the deficient mediator nitric oxide, and prostacyclin derivatives provide an exogenous supply of the deficient mediator prostacyclin.[4] Combining these molecular targets makes intuitive sense, because all of these pathways are intimately involved in disease progression. A similar strategy of combining molecular targets has been very successful in the management of patients with chronic heart failure from left ventricular systolic dysfunction, where combination therapy is the standard of care.

Figure 3.  (click image to zoom)

Molecular targets for therapy in pulmonary arterial hypertension.
From: Humbert M, Sitbon O, Simonneau G. Treatment of pulmonary arterial hypertension. N Engl J Med. 2004;351:1425-1436. The New England Journal of Medicine (c) 2004.      

  Printer- Friendly Email ThisReferencesRubin LJ. Diagnosis and management of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest. 2004;126:7S-10S. AbstractWagenvoort CA, Wagenvoort H. Primary pulmonary hypertension: a pathologic study of the lung vessels in 156 classically diagnosed cases. Circulation. 1970;42:1163-1184.Gaine SP, Rubin LJ. Primary pulmonary hypertension. Lancet. 1998;352:719-725. AbstractHumbert M, Sitbon O, Simonneau G. Treatment of pulmonary arterial hypertension. N Engl J Med. 2004;351:1425-1436. AbstractBadesch DB, Abman SH, Ahearn GS, et al. Medical therapy for pulmonary arterial hypertension: ACCP evidence-based practice guidelines. Chest. 2004;126:35S-62S. AbstractRich S, Seidlitz M, Dodin E, et al. The short-term effects of digoxin in patients with right ventricular dysfunction from pulmonary hypertension. Chest. 1998;114:787-792. AbstractRich S, Kaufmann E, Levy PS. The effect of high doses of calcium-channel blockers on survival in primary pulmonary hypertension. N Engl J Med. 1992;327:76-81. AbstractSitbon O, Humbert M, Jais X, et al. Long-term response to calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation. 2005;111:3105-3111. AbstractChannick RN, Simonneau G, Sitbon O, et al. Effects of the dual endothelin receptor antagonist bosentan in patients with pulmonary hypertension: a randomized, placebo-controlled study. Lancet. 2001;358:1119-1123. AbstractRubin LJ, Badesch DB, Barst RJ, et al, for the Bosentan Randomized Trial of Endothelin Antagonist Therapy Study Group. Bosentan therapy for pulmonary arterial hypertension. N Engl J Med. 2002;346:896-903. AbstractMcLaughlin VV, Sitbon O, Badesch DB, et al. Survival with first-line bosentan in patients with primary pulmonary hypertension. Eur Respir J. 2005;25:244-249. AbstractHoeper MM. Drug treatment of pulmonary arterial hypertension: current and future agents. Drugs. 2005;65:1337-1354. AbstractWilkins MR, Paul GA, Strange JW, et al. Sildenafil versus endothelin receptor antagonist for pulmonary hypertension (SERAPH) study. Am J Respir Crit Care Med. 2005;171:1292-1297. AbstractOlschewski H, Simonneau G, Galie N, et al, for the Aerosolized Iloprost Randomized Study Group. Inhaled Iloprost for Severe Pulmonary Hypertension N Engl J Med. 2002;347:322-329.Simmoneau G, Barst RJ, Galie N, et al, for the Treprostinil Study Group. Am J Respir Crit Care Med. 2002;165:800-804. AbstractGomberg-Maitland M, Tapson VF, Benza RL, et al. Transition from intravenous epoprostenol to intravenous treprostinil in pulmonary hypertension. Am J Respir Crit Care Med. 2005 Sep 8 [epub ahead of print].Barst RJ, Rubin LJ, Long WA, et al, for The Primary Pulmonary Hypertension Study Group. N Engl J Med. 1996;334:296-301. AbstractMcLaughlin VV, Shillington A, Rich S. Survival in Primary Pulmonary Hypertension: The Impact of Epoprostenol Therapy. Circulation. 2002;106:1477-1482. AbstractSitbon O, Humbert M, Nunes H, et al. Long-term intravenous epoprostenol infusion in primary pulmonary hypertension: prognostic factors and survival. J Am Coll Cardiol. 2002;40:780-788. AbstractKao PN. Simvastatin treatment for pulmonary hypertension: an observational case series. Chest. 2005;127:1446-1452. AbstractHumbert M, Barst RJ, Robbins IM, et al. Combination of bosentan with epoprostenol in pulmonary arterial hypertension: BREATHE-2. Eur Respir J. 2004;24:353-359. AbstractGhofrani HA, Wiedemann R, Rose F, et al. Combination therapy with oral sildenafil and inhaled iloprost for severe pulmonary hypertension. Ann Intern Med. 2002;136:515-522. AbstractWilkens H, Guth A, Konig J, et al. Effect of inhaled iloprost plus oral sildenafil in patients with primary pulmonary hypertension. Circulation. 2001;104:1218-1222. AbstractGhofrani HA, Rose F, Schermuly RT, et al. Oral sildenafil as long-term adjunct therapy to inhaled iloprost in severe pulmonary arterial hypertension. J Am Coll Cardiol. 2003;42:158-164. AbstractHoeper MM, Faulenbach C, Golpon H, Winkler J, Welte T, Niedermeyer J. Combination therapy with bosentan and sildenafil in idiopathic pulmonary arterial hypertension. Eur Respir J. 2004;24:1007-1010. AbstractPaul GA, Gibbs JS, Boobis AR, Abbas A,Wilkins MR. Bosentan decreases the plasma concentration of sildenafil when coprescribed in pulmonary hypertension. Br J Clin Pharmacol. 2005;60:107-112. Abstract

Medscape Cardiology.  2005;9(2) ©2005 Medscape
This is a part of article Combination Therapy: The Future of Medical Management for PAH Taken from "Disfunction Erectile" Information Blog

Friday, July 04, 2008

Intracavernosol Injection Algorithm


Abstract and Introduction


Intracavernosal injections provide an effective therapy for men with erectile dysfunction who can not take oral agents or for whom oral agents are not effective. Determining the best initial dosage can be a challenge for health care providers. A literature review and 13 years of experience working with patients receiving intracavernosal injections provide the basis for the algorithm designed to provide guidance with the dosage and titration of the injection medications.Introduction

Intracavernosal injection therapy is an effective therapy for men with erectile dysfunction (ED) who can not take oral agents or for whom oral agents are not effective. Initial dosing and dosage titration is typically individualized for each man, but there are general guidelines that can be followed. In caring for men who are beginning therapy with intracavernosal penile injections, the health care clinician is faced with many choices about starting dosages and titration of medications.

Injections are given with a 1 ml syringe with 1/2 or 5/8-inch length, and a 27 to 30-gauge needle. The injection may be given anywhere from the base of the penis to two-thirds of the way down the penile shaft at the 10 o'clock and 2 o'clock locations on the upper side of the penis away from the urethra and the head of the penis (see Figure 1). Injections are rotated within that area and the side of the injection is alternated with each injection. Many factors must be considered when determining a starting dose and titrating medication for patients. The goal of this treatment is to create an erection sufficient for sexual relations, while minimizing side effects such as pain or priapism.

Figure 1.  (click image to zoom)

Intracavernosal Injection Sites illustrated in shaded area.      

  Printer- Friendly Email ThisReferencesBaniel, J., Israilov, S., Engelstein, D., Shmueli, J., Segenreich, E., & Livne, P.M. (2000). Three-year outcome of a progressive treatment program for erectile dysfunction with intracavernous injections of vasoactive drugs. Urology, 56(4), 647-652Bennett, A.H., Carpenter, A.J., & Barada, J.H. (1991). An improved vasoactive drug combination for a pharmacological erection program. Journal of Urology, 146(6), 1564-1565Brindley, G.S. (1986). Pilot experiments on the actions of drugs injected into the human corpus cavernosum penis. British Journal of Pharmacology, 87(3), 495-500Brock, G., Tu, L.M., & Linet, O.I. (2001). Return of spontaneous erection during long-term intracavernosal alprostadil (Caverject) treatment. Urology, 57(3), 536-541Goldstein, I., Auerbach, S., Padma-Nathan, H., Rajfer, J., Fitch, W., & Schmitt, L. (2000). Axial penile rigidity as primary efficacy outcome during multi-institutional in-office dose titration clinical trials with alprostadil alfadex in patients with erectile dysfunction. Alprostadil alfadex study group. International Journal of Impotence Research, 12(4), 205-211Kuan, J.K., & Brock, G.B. (2001). Salvage of the sildenafil non-responder: The role of locally delivered therapies. Sexual Dysfunction in Medicine, 2(2), 34-39Linet, O.I., & Ogring, F.G. (1996). Efficacy and safety of intracavernosal alprostadil in men with erectile dysfunction. New England Journal of Medicine, 334(14), 873-877Montorsi, F., Salonia, A., Zanoni, M., Pompa, P., Cestari, A., Guazzoni, G., et al. (2002). Current status of local penile therapy. [review] [80 refs]. International Journal of Impotence Research, 14(Suppl. 1), S70-81Mulhall, J.P., Jahoda, A.E., Cairney, M., Goldstein, B., Leitzes, R., Woods, J., et al. (1999). The causes of patient dropout from penile self-injection therapy for impotence. Journal of Urology, 162(4), 1291-1294Pharmacia. (2002). Caverject Impulse prescribing information. Kalamazoo, MI:Pharmacia and UpJohnPorst, H., Buvat, J., Meuleman, E., Michal, V., & Wagner, G. (1998). Intracavernous alprostadil alfadex – an effective and well tolerated treatment for erectile dysfunction. Results of a long-term European study. International Journal of Impotence Research, 10(4), 225-231Richters, S., Vardi, Y., Ringel, A., Shavel, M., & Nissenkorn, I. (2001). Intra venous injections: Still the gold standard for treatment of erectile dysfunction in elderly men. International Jouranl of Impotence Research, 13, 172-175Schwarz Pharma. (2004). Edex (alpro stadil). Prescribing information. Milwaukee, WI:Schwarz PharmaSeyam, R., Mohamed, K., Akhras, A.A., & Rashwan, H. (2005). A prospective randomized study to optimize the dosage of trimix ingredients and compare its efficacy and safety with prostaglandin E1. International Journal of Impotence Research, 7, 346-353

Urol Nurs.  2006;26(6):449-453.  ©2006 Society of Urologic Nurses and Associates
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Pulmonary Arterial Hypertension: Current Therapeutic Strategies


Choice of Therapy

The decision of which agent to use is largely dependent on the severity of PAH at presentation and, to some extent, on patient preference. In patients who are WHO functional class I-II at presentation, an oral agent, such as an endothelin-receptor antagonist or phosphodiesterase inhibitor, is usually an appropriate first choice and often results in symptomatic improvement. For patients who present with evidence of right heart failure or right ventricular dysfunction, a parenteral agent (typically epoprostenol or a prostacyclin analog) can be appropriate, but the initiation of oral agents should also be considered. Increasingly, many patients are hesitant to consider a parenteral agent in the face of available oral agents; however, no long-term data exist regarding the use of the oral agents in patients with severe right ventricular dysfunction.Previous PageSection 7 of 10 Nat Clin Pract Cardiovasc Med. 2007; 4(6):319-329. ©2007  Nature Publishing Group
This is a part of article Pulmonary Arterial Hypertension: Current Therapeutic Strategies Taken from "Disfunction Erectile" Information Blog

Thursday, July 03, 2008

COX-2 Inhibitors and The Cardiovascular System: A Class Effect?



It seems clear that rofecoxib stands out amongst the COX-2 inhibitors as carrying a greater risk of thrombotic cardiovascular events, oedema and loss of blood pressure control in treated hypertensive patients when compared to classical NSAIDs. The increase in cardiovascular risk is greatest after about 18 months of use, and many of the newer COX-2 inhibitors have not been studied adequately over such prolonged periods. However, the emerging data suggest that the increased cardiovascular risk is probably a class effect, although the absolute risk with drugs other than rofecoxib is small. There may also be a dose-related increase in risk with some drugs, particularly celecoxib and valdecoxib, with the greatest risk at doses higher than those usually used for the treatment of arthritis.

Currently, the Medicines and Healthcare Regulatory Agency (MRHA) recommend avoiding treatment with COX-2 selective inhibitors whenever possible in patients with known ischaemic heart disease or those who are at high risk of developing it. They also recommend that the smallest dose of a COX-2 inhibitor should be prescribed for the shortest possible duration if the drugs are used. The risk associated with the use of meloxicam, a drug with less COX selectivity, has received less attention. Current evidence has not demonstrated any differences from conventional NSAIDs, but definitive studies are awaited.

If the prescription of COX-2 selective inhibitors is considered for patients with ischaemic heart disease, then a full discussion of risk should take place, and all alternative treatment options should be explored. The long-term use of COX-2 inhibitors for patients at lower cardiovascular risk should also be reassessed in the light of the lack of evidence for a reduction in serious gastrointestinal toxicity for many of the drugs compared with classical NSAIDs.  Printer- Friendly Email ThisReprint Address

Correspondence to: Dr DG Waller (email: derek.waller@suht.swest.nhs.uk )

Br J Cardiol.  2005;12(5):387-391.  ©2005 Sherborne Gibbs Ltd.
This is a part of article COX-2 Inhibitors and The Cardiovascular System: A Class Effect? Taken from "Generic Arcoxia (Etoricoxib)" Information Blog

An Update on Transient Ischemic Attacks



Healthcare professionals want the best outcomes for people who have had TIA. Achieving better outcomes includes being knowledgeable about the proposed definition of TIA and the aggressive work-up recommended. Patient and family members need to be knowledgeable about anticoagulant and antiplatelet agents, surgical procedures, and risks so that all can work together to prevent a recurring TIA and possible future stroke.CE Information

The print version of this journal was originally certified for CE credit, For accreditation details, please contact the publisher, American Association of Neuroscience Nurses (AANN) 4700 W. Lake Avenue, Glenview, IL 60025-1485.  Printer- Friendly Email ThisReprint Address

Janice Hinkle, PhD RN CNRN, Acute Stroke Programme, Nuffield Department of Clinical Medicine, Level 7, John Radcliffe Hospital, Headington, Oxford, England OX3 9DU, or via e-mail at janice.hinkle@ndm.ox.ac.uk .

J Neurosci Nurs.  2005;37(5):243-248.  ©2005 American Association of Neuroscience Nurses
This is a part of article An Update on Transient Ischemic Attacks Taken from "Disfunction Erectile" Information Blog