One woman’s war with fake drugs

Counterfeit drugs are flooding the international marketplace, but Nigeria's Dr Dora Akunyili fights day and night to stop it.

Dora is angry.

Angry because her diabetic sister died from what she is convinced were fake insulin and fake antibiotics.

And angry because so many of her countrymen and women are fighting killer diseases like malaria and tuberculosis with little more than sugar syrup and chalk tablets, cynically packaged to look like the real thing.

When she started her job as director general of Nigeria's National Agency for Drug and Food Administration (Nafdac), she trawled drugs markets, hospitals and clinics and was horrified at what she discovered.

A survey conducted with the World Health Organisation found more than half the drugs on sale in Nigeria were fake or sub-standard.

Nigeria's hospitals were using fake and contaminated drips, surgeons were using fake adrenalin to re-start the heart, anaesthetists were giving sub-strength muscle relaxant to patients in their operating theatres.

"Counterfeit drugs are murder," says Dora. "It is the highest form of terrorism against public health because it kills a mass."

Death threats

Until her arrival, Nafdac, like many other government organisations in Nigeria, had functioned little better than a toll gate. Importers simply paid a bribe to get their products into the market.

That changed.

Last year she closed down the vast open-air medicine market in Kano for three months, after her officers confiscated £140,000 worth of fake drugs.

But in a culture steeped in corruption, she has not had an easy ride.

She built a new team of female inspectors and pharmacists (she believes most men are too easily tempted by bribes) and started to prosecute importers of fake drugs.

When the public saw the dragons she was slaying, she may have become Nigeria's uncrowned queen, but the counterfeiters fought back.

They burnt down Nafdac's offices and threatened to kill her and her children.

When she stood firm, they shot her in her car. The bullet grazed her skull but she survived.

'Injecting water'

Direct proof that a fake drug has killed is hard to find.

However, one particular tragedy in July 2003, is probably as close as it gets.

The International Children's Heart Foundation visited Nigeria to operate on sick children at a teaching hospital in Enugu.

The operations should have been straightforward. The patients' prognosis was good. But when the operations began, things went wrong.

Cardiac nurse Joanne Price recalls: "You give them adrenalin to restart the heart and that normally works. But this time nothing came back. It was water. I felt we were basically injecting water instead of adrenalin."

Four children died as their parents watched and prayed.

Despite being confronted with what seemed to be a hospital cover-up, Dora confiscated supplies and found fake adrenalin, fake muscle relaxant and infected intravenous drips.

The hospital maintain there is no proof to link the deaths of the patients with the drugs used.

International effort

But the problem of fake drugs is not confined to Nigeria, or even the developing world.

In the UK in November 2004, Allan Valentine was imprisoned for manufacturing fake Diazepam and Viagra in his Wembley warehouse where Indian tablet presses and chemicals were found.

In the US, where patented drugs are the most expensive in the world, fakes have penetrated the pharmaceutical chain from drug manufacturers, through wholesalers, to high street pharmacies.

The American Food and Drugs Administration prosecutions have tripled in the last year.

At a conference in Paris about counterfeit medicines, Dora demands concerted global action. "Eradication of counterfeit drugs should be treated as an international health emergency," she says.

She believes that raising public awareness has produced dramatic results in Nigeria and urges other nations to be more open.

Unsurprisingly, drug companies around the world are fearful that their brand will be shunned if news of a fake gets out.

But no matter how tough the situation gets for pharmaceutical industry, Dora will not be leaving any stone unturned.

Bad Medicine was broadcast on Tuesday 12 July 2005 at 2100 BST on BBC Two.
This is a part of article One woman’s war with fake drugs Taken from "Sildenafil Citrate Generic" Information Blog

Pulmonary Hypertension in Heart Failure

Summary

Clinically important PH is common in patients with chronic HF. The optimal approach to these patients is uncertain and therefore must be individualized. When the PH is felt to be in proportion to the HF, therapy is generally focused exclusively on the HF. One exception is the patient with PH and advanced HF for whom mechanical circulatory support or cardiac transplantation is being considered. In this setting PAH-specific therapies may be a useful adjunct, possibly allowing for the potentially curative procedure to be attempted. When the PH is felt to be out of proportion to the HF, initial efforts are again focused on the HF. If the PH (and the symptoms potentially related to it) persists, and the PCWP is maintained in an acceptable range, the use of PAH-specific therapies may be considered. Caution must be used, however, because these agents may precipitate fluid retention and pulmonary edema in patients with HF. Whereas initial studies of PAH-specific therapies were discouraging, more recent ones have suggested promise. The results of several planned or ongoing trials in this area will undoubtedly lend clarity to this challenging clinical question. While awaiting those results, consensus statements from experts in the field will be forthcoming and should provide more guidance.

This activity is supported by an independent educational grant from Actelion.  Printer- Friendly Email ThisAcknowledgements

The author would like to thank Drs. Myung Park and Jeffrey Teuteberg for their critical reviews and suggestions.

Medscape Pulmonary Medicine.  2008; ©2008 Medscape
This is a part of article Pulmonary Hypertension in Heart Failure Taken from "Sildenafil Citrate Generic" Information Blog

The Present and Future Role of Aldosterone Blockade

Conclusion

In addition to the traditional effects of aldosterone on fluid and sodium retention, a range of newly-recognised effects of aldosterone contribute to its detrimental effect on cardiovascular events, in particular on sudden death. Apart from the well-recognised effect of potassium and magnesium depletion, preclinical and clinical studies have shown that aldosterone promotes endothelial function and cardiac fibrosis, actions which would be expected to play an important part in promoting cardiac events.

We now have convincing clinical evidence that these effects translate to a significantly harmful effect of aldosterone in patients with CHF. Large-scale prospective studies have reported a marked and significant benefit from use of an aldosterone blocker in terms of overall mortality, cardiovascular mortality (particularly sudden death) and hospitalisation. In one trial, these improvements were seen even when patients were already taking an ACE inhibitor and a beta blocker in addition to aldosterone blockade. Optimal therapy for patients with congestive heart failure should now routinely include an aldosterone blocker since two major trials clearly documented a highly significant reduction in total mortality by doing so.

Reprint Address

Correspondence to: Professor AD Struthers (email: a.d.struthers@dundee.ac.uk)Previous PageSection 5 of 5Br J Cardiol 11(1):56-60, 2004. © 2004 Sherborne Gibbs Ltd.
This is a part of article The Present and Future Role of Aldosterone Blockade Taken from "Aldactone Spironolactone Acne" Information Blog

Rules of Evidence: CMS and Primary Prevention of Sudden Cardiac

The CMS Recommended ICD in Primary Prevention Patients

The CMS Decision Summary specifies reimbursement to be restricted to single chamber "shock only" ICDs unless physician documentation of need for more sophisticated ICD therapy is provided. These statements demonstrate a fundamental misunderstanding of basic ICD system operation, and specifically, those ICDs used in SCD-HeFT. The simple fact is that there is no "SCD-HeFT" ICD. The SCD-HeFT investigational plan specified ICD programming with a single detection zone and high-voltage therapies. However, all contemporary ICD systems, including those used in SCD-HeFT, are capable of delivering antitachycardia pacing (ATP) for painless termination of VT. Numerous older studies have consistently demonstrated that ATP can reliably terminate ~85–90% of slow VT (cycle lengths [CL] <300–320 ms) with a low risk of acceleration (1–5%).[25] More recently similar high success and low acceleration rates for fast VT (CL 320–240 ms) have been demonstrated.[26,27] Furthermore, the majority of true ventricular detections in both primary and secondary prevention ICD patients are due to VT and fast VT; true VF accounts for only ~10% of total episodes in both groups.[28] There was no difference in the relative frequency of VT, FVT, or VF between primary and secondary prevention groups. Furthermore, there was was no difference in cycle lengths of VT or FVT between groups.[28] It would be a step backwards to withhold painless termination for more than 70% of all episodes of VT. Painful shocks remain a significant problem for ICD patients and may be psychologically incapacitating, particularly if they occur sequentially within a short time span (ICD storm).[29] Several studies have noted a direct correlation between poor quality of life (QoL) scores and the experience of ICD shocks.[29–33] Furthermore, reduction of painful shocks by ATP has been shown to improve QoL[34] and may extend pulse generator longevity. These observations have repositioned the ICD as primarily an ATP device with defibrillation back up only as needed. The implementation of ATP in ICD platforms does not contribute significantly to cost.  Printer- Friendly Email This

Pacing Clin Electrophysiol.  2005;28(2):81-88.  ©2005 Blackwell Publishing
This is a part of article Rules of Evidence: CMS and Primary Prevention of Sudden Cardiac Taken from "Aldactone Spironolactone Acne" Information Blog

Effect of Once Daily Alfuzosin on Urinary Symptoms

Discussion

The Fifth Consultation on BPH and the latest American Urological Association (AUA) guidelines[4,18,19] indicate that the goal of therapy for LUTS in BPH is to improve symptomatology concomitantly with quality of life. BPH is a chronic disease and patient compliance is important in achieving efficacy of treatment.[18] LUTS are present over 24 hours, and it is possible to obtain good control of symptoms if therapy is maintained for 24 hours.[4,18,19] Otherwise these patients usually prefer non-invasive treatments and specifically pharmacological therapy.[3]

The clinical efficacy and safety of a1-blockers in symptomatic patients with BPH is well documented. Different studies demonstrate a rapid improvement in flow rates and a rapid relief of urinary symptoms after treatment with alfuzosin 2.5 or 5mg twice daily.[20-22] Long-term benefits, such as maintenance of symptom relief, reduction in the incidence of acute urinary retention, and a low incidence of sexual and cardiovascular adverse effects, were also demonstrated.[20-22] Recently, a new once-a-day alfuzosin formulation has become available that seems to improve the efficacy and tolerability of the earlier formulation.[4] Van Kerrebroeck et al. demonstrated that alfuzosin 10mg OD is an effective treatment for LUTS and is associated with improvements in symptoms and flow rates for up to 12 months of treatment compared with placebo.[23]

The present study confirms the efficacy of alfuzosin in terms of providing symptom relief and improvements in urinary flow parameters. In particular, we observed a significant reduction (39.5%) in urinary symptoms, assessed by I-PSS after a week of treatment with alfuzosin OD. This finding compares well with Djavan and Marberger's investigation of a-blocker efficacy (30-40% reduction in symptoms).[24] Furthermore, while studies have evaluated drug effects on urinary flow rates by means of office uroflowmetry, no previous clinical study has investigated 24-hour efficacy assessed by home-based measurement of maximum flow. Verification of efficacy over 24 hours is important to ensure good patient compliance.[16] Many patients are not able to void at the clinic as they do normally. The patient has to void in an environment that can be very embarrassing and requires a bladder full enough to obtain a representative volume.[25] Variability between consecutive flow measurements may also be found in the clinic. Multiple office samples taken in privacy, at different times of the day when voiding is felt, has also been proposed. Unfortunately, this situation is difficult to accomplish and time consuming. A home uroflowmeter (P-Flow) evaluation as proposed by de La Rosette et al.[16] may provide reliable results.

In the present study, home flowmetry showed that alfuzosin 10mg OD produced a significant improvement in terms of Qmax and voiding volume. In particular, it is clinically relevant that alfuzosin 10mg OD led to an improvement in Qmax of 36% after 8 hours and of 33% after 24 hours. These data show that alfuzosin is effective after the first dose and its efficacy is maintained over 24 hours with an improvement in Qmax that compares well with that reported by Djavan and Marberger (16-25%).[24] Our data are also supported by Marks et al.,[26] who demonstrated in a uroflowmetry study a similar Qmax improvement 8 hours after the first dose and after 4 days of treatment using the same OD alfuzosin formulation as in the current study. Geomatrix® technology guarantees a longer median time to Cmax (tmax) values; in fact, these are longer for the OD formulation (4.0-16.0h) than for the 2.5mg three-times-daily or 5mg twice-daily formulations (0.5-1.5h).[27] This evidence demonstrates that alfuzosin OD exhibits a urodynamically measurable effect within hours of the first dose and maintains this level over 24 hours, thus avoiding the necessity to obtain steady state.

Improvement in flow rates seems to be related to alfuzosin treatment, and changes in Qmax observed at different evaluations during the same day of treatment should be related to the circadian changes in urinary pattern. Mean Qmax recorded at different times during the day during treatment was always higher than mean Qmax recorded at the same time of day during the baseline assessment in our study.

The present study appears to clinically confirm the pharmacokinetic studies of alfuzosin 10mg OD, demonstrating that it ensures 24-hour coverage with a delay in tmax compared with alfuzosin 5mg twice daily.[28] A peak plasma concentration of alfuzosin was observed 8 hours after the administration of alfuzosin 10mg OD compared with after 3 hours for alfuzosin 5mg twice daily.[28] According to the plasma concentration profiles, alfuzosin 10mg OD should be clinically effective over 24 hours as observed in our study by means of improvement in urinary flow rates.

Limitations of our study include the small group of patients evaluated. However, it should be taken into account that about 300 urinary flows were analysed and screened for artefacts, and that home flowmetry is a time-consuming procedure not easily performed for a large series of data. Furthermore, the Fifth Consultation on Benign Prostatic Hyperplasia recommends further research into the potential benefits of home flowmetry and into its role in assessing new medical treatment.[29]  Printer- Friendly Email This

Clin Drug Invest.  2005;25(6):359-365.  ©2005 Adis Data Information BV
This is a part of article Effect of Once Daily Alfuzosin on Urinary Symptoms Taken from "Cheap Finasteride Propecia" Information Blog

Choose your favourite model of slutty videos.

Choose your favourite model of slutty videos. I also recommend watch free blue movie online pics.

The investigators examined the database

The investigators examined the database for ICD-9 code
008.45 between January 2004 and June 2005, selecting those patients
whose chemist’s shop evidence indicated direction with oral MET or oral
VANC, with the gain of a “suspected oral VANC” abstract entity.
This last was defined as a shop record book for intravenous VANC
without grounds of accompanying intravenous giving medication (seen
with almost 50% of VANC), as outpatient oral VANC use in the United
States is often via the cheaper intravenous creating by mental acts.
Patients who were excluded had no CDAD therapy (8.9%), simultaneous MET
and VANC therapy (1.9%), or intravenous MET as honours therapy (4.0%).
The researchers found that there was a much greater use of first-line
MET (n = 28,905) compared with VANC (n = 3420).
Patients receiving first-line MET and VANC were a mean age of 70.2
assemblage and 70.5 gathering, respectively, and 42.1% vs 37.3% were men (P < .0001).
Relation of the All Case Refined-Diagnosis Related Group (APR-DRG) intensity of illness ratings showed a significant way (P
< .0001) for MET use for more severe disease.
This was also reflected in the “extremely ill” cows 4 asperity,
represented by 30.5% of the MET unit and 24.1% of the VANC abstraction.
“However, as you would expect,” Dr.
Davidson said, “more vancomycin patients had a knowledge of a prior
CDAD entree.” This reached import, with 10.4% of those treated with MET
and 30.7% of those treated with VANC (P
< .0001), and the VANC building block was also slightly more likely
to have had prior acid suppressive therapy (42.1% vs 53.1%,
respectively; P < .0001). The intensive care unit (ICU)
fundamental measure of stay was similar between MET and VANC groups
(6.8% vs 6.6%), although MET use required a significant histrion day in
healthcare facility (12.8 vs 11.5 days; P < .0001). Regarding outpouring outcomes, Dr.
Davidson noted that they were not adjusted for comorbidities: “Here we see that patients seemed to buy metronidazole online do less well than vancomycin patients” (MET vs VANC): destruction, 7.9% vs 6.8% (P < .0001); ICU stay, 23.2% vs 17.7% (P < .0001); additional care on shooting, 31.0% vs 29.4% (P = .049). Although MET cost less than VANC per expelling ($90 vs $375; P
<.0001) and the sum chemist’s shop costs were similar ($2439 vs
$2492), the amount healthcare facility cost per emanation was
significantly greater for patients in the MET chemical group ($16,953
vs $14,718; P < .0001). Thus, although this document
highlighted a figure of problems associated with the selection of
first-line direction of CDAD, as Dr.
Davidson stressed, “Clearly further inquiry is required to compare
discussion outcomes of CDAD therapies and to controller for
patient-level factors.” Join 17th European Meeting of Clinical
Microbiology and Infectious Diseases and 25th International Coition of
Chemotherapy: Conception O331.
This is a part of article The investigators examined the database Taken from "Cheap Finasteride Propecia" Information Blog