Fluoroquinolone Antibiotics And Neuropathy A Report

Today's important post from the Journal of Investigative Medicine at hic.sagepub.com (see link below) is another piece of the jigsaw showing how dangerous fluoroquinolone antibiotics can be for people whether living with, or prone to, nerve damage (neuropathy). It's quite long but worth reading because it's very important to check what sort of antibiotics your doctor is prescribing. Permanent neuropathy from an antibiotic is no joke and is so easily avoided - it's in your own interests to check the label on the box and question your doctor's choice afterwards.
 

Permanent Peripheral Neuropathy
A Case Report on a Rare but Serious Debilitating Side-Effect of Fluoroquinolone Administration
Published July 27, 2014, doi: 10.1177/2324709614545225 Journal of Investigative Medicine High Impact Case Reports April-June 2014 vol. 2 no. 2 2324709614545225

Jacquelyn K. Francis, BA1
Elizabeth Higgins, MD1
1Albany Medical College, Albany, NY, USA
Jacquelyn K. Francis, Albany Medical College, 47 New Scotland AvenueAlbany, NY 12208, USA. Email: francij@mail.amc.edu

Abstract

The health risks and side effects of fluoroquinolone use include the risk of tendon rupture and myasthenia gravis exacerbation, and on August 15, 2013, the Food and Drug Administration updated its warning to include the risk of permanent peripheral neuropathy. We present a case of fluoroquinolone-induced peripheral neuropathy in a patient treated for clinically diagnosed urinary tract infection with ciprofloxacin antibiotic.

Introduction

While there has been success in recent years in decreasing the numbers of unnecessary antibiotic administrations,1 still rampant in medical practice is the inappropriate use of antibiotics. Fluoroquinolones administration is no different. These bactericidal agents are capable of central nervous system (CNS) penetration,2 with an impressive treatment profile that includes an enhanced spectrum of activity, high oral bioavailability, high serum drug concentration that parallels that of intravenous drug administration, and rapid mechanism of action. It is for this reason that physicians favor these drugs for treatment of simple infections, which range from uncomplicated urinary tract infections (UTIs) and gastrointestinal infections to lower respiratory infections and pneumonias. According to established guidelines, however, these antibiotics are recommended as drugs of last resort and for treatment of cases refractory to other safer antibiotic alternatives. Reports in recent years of the adverse drug events of these drugs are on the rise, with not only an overrepresentation of common antibiotic complaints, including diarrhea, nausea, and headache that occur at rates higher than most other antimicrobials on the market,3 but there is also mounting evidence suggesting the potential for long-term adverse peripheral nervous system (PNS) effects from fluoroquinolone usage. The need for physicians to be judicious when prescribing these drugs is therefore paramount.

Case Presentation

A 57-year-old Caucasian female presented to outpatient clinic with complaints of dysuria, polyuria, and urinary urgency. Urinalysis showed 2+ leukocytes and trace blood. Based on her clinical presentation, she was treated for UTI with a ciprofloxacin regimen of 250 mg twice a day for 5 days. Subsequent urine culture showed no evidence of organism, and against advice for reevaluation, she was lost to follow-up. She presented 2 months later reporting whole body burning and alopecia. The burning, she claimed, started 2 or 3 days after completion of the prescribed course of ciprofloxacin. The burning lasted 3 weeks and resolved only to recur, unrelentingly, 3 weeks later. She had been unable to adorn clothing during this time, for she said this triggered whole body burning. At the point wherein she was finally able to wear clothing, she presented to the clinic. Hydration and Epsom salt soaks provided no relief. She reported pain of 10/10. Her past medical history is significant for trigeminal neuralgia, in remission for 12 years. The patient was on no medications at the time of her visit. She has no specific medication allergies, but does get gastrointestinal symptoms with opioids, namely, fentanyl. Physical examination was unremarkable. Vitals at the time that she was seen included the following: blood pressure 132/78 mm Hg, temperature of 97°F, heart rate of 60 beats per minute, respirations of 18. Her body mass index was 17.94, down from 20.3 two months earlier. On detailed neurologic examination, cranial nerves II through XII were intact bilaterally. There was no pronator drift of outstretched arms. There was some muscle wasting in biceps; however, overall tone was normal. Strength was full bilaterally. Reflexes were 2+ and symmetric at the biceps, triceps, knees, and ankles. Plantar responses were flexor. Light touch and pinprick produced pain and paresthesias diffusely in the upper and lower extremities; however, position sense and vibration sense were intact in fingers and toes. Rapid alternating movements and fine finger movements were intact. There was no dysmetria on finger-to-nose and heel-knee-shin. There were no abnormal or extraneous movements. Romberg was absent. The patient’s posture was normal. Gait was steady with normal, though tentative, steps, base, arm swing, and turning. Heel and toe walking were normal. Tandem gait was normal. She had no discernable rash or skin lesions.

Subsequent complete blood work analysis to check for an electrolyte abnormality basis of her complaints was unremarkable. Her complete blood count was normal with a hematocrit of 41%. Her vitamin B12 level was 258 pg/mL, with a normal range of 200 to 900 pg/mL. Her thyroid stimulating hormone level was 2.05, with a normal range of 0.4 to 6.0. Her immunoglobulin levels were normal. Her vitamin D level was 13 nmol/L (optimal >30 nmol/L). Copper level was 98 mg (normal 50-80 mg). Vitamin E was normal at 12.7 µg/mL (normal range = 5.5-17 µg/mL). Vitamin B1 was normal at 5.4 µg/dL (normal range = 2.5-7.5 µg/dL).

Her blood work and further questioning could provide no new medical etiology for her symptoms, and so the patient was subsequently sent for complete neurological workup. Workup included heavy metal toxicity screening to assess for possible heavy metal exposure to lead, mercury, cadmium, and zinc. Electrophysiological studies were also done to assess neuromuscular nerve action potential transmission, a test that could discern a neuromuscular disorder etiology. Three-millimeter skin punch biopsy to assess for small fiber density and possible neurologic process were also done. These tests were all negative. Neurological workup could not determine a unique cause of her symptoms. It was concluded that if her symptoms were neurologic-based, it was, in fact, a multifocal process.

Two years after the initial onset of symptoms, the patient continues to suffer from polyneuropathies chronologically related to ciprofloxacin use. At her most recent visit, she describes constant pain of 7/10 and is unable, she states, to ambulate for more than 2 minutes, without intense shooting pains up and down her lower extremities. She describes “pins and needles” up and down her legs and thighs radiating to her buttocks and feet. She claims that her upper body and abdomen have now been spared of such feelings. She describes severe alopecia and ambulates now with a broad-based gait. She describes being on permanent disability because of her condition. The rest of her physical examination remains unchanged. There are no gross neurological deficits discernible on neurologic examination. The patient remains on amitriptyline 20 mg daily for control of her pain symptoms.

Discussion

Fluoroquinolones are fluorinated quinolones, the only bactericidal agent in the antibiotic class capable of directly inhibiting DNA synthesis. They do this by promoting cleavage of bacterial DNA in the DNA–enzyme complexes of DNA gyrase and topoisomerase IV.2 Generally, gram-negative antibacterial activity correlates with inhibition of DNA gyrase, and gram-positive antibacterial activity corresponds with inhibition of DNA type IV topoisomerase.2,4 With the introduction of these drugs in the 1960s, physicians were able, for the first time, to treat severe gram-negative infections orally.3 The first successful fluorination of part of the quinolone drug in 1986, in the form of norfloxacin, brought with it the capability of crossing the blood–brain barrier and achieving CNS penetration.5 This and the already great treatment profile in the form of enhanced spectrum of activity, high oral bioavailability, high serum drug concentration comparable to intravenous infusion, and rapid mechanism of action added to the popularity of these drugs ultimately resultingin the indiscriminate use of these drugs. The enhanced treatment profile of these drugs came at a price however, with adverse effects so severe that use of many fluoroquinolones since then being restricted or the drugs withdrawn from the market entirely.6,7

One of the challenges of diagnosing a patient with fluoroquinolone-associated peripheral neuropathy is the diffuse, confusing, and delayed array of symptoms that can occur. A 1996 study first brought these adverse effects to light.7 While patients on the fluorinated drugs exhibited less side effects than those associated with first-generation quinolone predecessors, such as nausea and gastrointestinal disturbances, 0.9% to 1.6% experienced adverse reactions relating to the peripheral and central nervous system, including headache, dizziness, drowsiness, agitation, psychosis, and convulsions, as well as peripheral sensory disturbances, symptoms that had never been complained of prior, at least not on any significant scale. Of these patients, 81% had symptoms occurring within 1 week of drug administration, with paresthesia being the mainly reported symptom. Five years later, a 2001 study found that contrary to previous reports suggesting that fluoroquinolone-associated PNS events are mild and short term, 80% of study participants reported severe events that typically involved multiple organ systems, especially the PNS, with symptom onset as early as 24 hours within initiation of treatment. 58% of these cases had symptoms lasting greater than 1 year.8

Another 2001 formal study that sought to assess the prevalence of fluoroquinolone-induced PNS adverse side effects highlighted the severity of these effects. The study concluded that there was a high association between fluoroquinolone antibiotics and severe, long-term adverse PNS and multiple organ system effects that included PNS sensory symptoms (91%), peripheral neuropathy motor symptoms (55%), and CNS effects (75%). Over 80% of the patients surveyed had sequalae stemming from fluoroquinolone use that lasted for greater than 1 year.9 A subset of these patients and their adverse drug events are included in Table 1.


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Table 1.

15 of the 45 Total Reported Cases of Fluoroquinolone-Associated Events in the Literature6.

Despite these seemingly significant numbers and overwhelming reports from patients, physicians continue to prescribe fluoroquinolone antibiotics unsystematically, against US Food and Drug Administration recommendations. The pressures of health care facilities and patients alike to increase patient turnaround and quickly alleviate symptoms may compound this problem 10.

As highlighted in the aforementioned case, the peripheral neuropathy reported with fluoroquinolone administration can be severe, debilitating, and permanent. It is for this reason that physicians need to practice due diligence when prescribing not only antibiotics, but any drug. Physicians also need to practice vigilance in the event of an adverse reaction. They can do this with careful follow-up of patients and ensure that patients are aware of all the side effects that may be associated with their prescribed drug. Patients need to know what to look for and where to go in the event that one of these symptoms become manifest. It is our hope that the updated FDA warning and presentation of this case will encourage physicians to be more conscientious of their treatment selections.

Take Home Points

The FDA recommends that fluoroquinolones be used as a drug of last resort and for treatment of cases refractory to other safer antibiotic alternatives.

The FDA updated their black box warnings on all fluoroquinolones to stress the rapidity of onset and permanence of peripheral neuropathy associated with their use.

Physicians should be aware of the risks and side effects associated with the drugs that are prescribed and be able to inform patients of the risks associated with the use of these drugs.

Physicians should always aim to administer the least broad spectrum antibiotic possible based on known sensitivities and regional resistance patterns.

Article Notes

Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.

This article is distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (http://www.uk.sagepub.com/aboutus/openaccess.htm).

References
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Scheld M. Quinolone therapy for infections of the central nervous system. Rev Infect Dis. 1989;11(suppl 5):S1194-S1202.
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http://hic.sagepub.com/content/2/2/2324709614545225.full

Neuropathy And HIV A Progress Report 2011 2012

 Today's long post via positivelite.com (see link below) was written by the moderator of this blog as a means of summing up the progress in neuropathy treatment over the past 18 months. There's a lot of information but it should give you an idea of what's going on in the research labs of the major  pharmaceutical companies and give you some hope that eventually, a treatment will emerge that will suit you as an individual with neuropathic problems.


Neuropathy and HIV: A Progress Report

Friday, 09 November 2012 Author // Dave R

Dave R writes...Neuropathy affects up to 40% of all people with HIV, yet the treatment has remained more or less the same for decades. Prescribing drugs meant for other diseases, has led to haphazard results; time for a change - but is it happening?
Couple the conditions neuropathy and HIV-infection together and in 2012, you have more people than ever who understand what you’re talking about. Growing older and surviving with HIV seems to mean the increase of long-term, age or HIV-related, side-effect conditions like neuropathy. To save time in relation to this article; much more information about the disease and its links to HIV can be found in other articles here, here and here.


It’s an infuriating and frustrating problem for both patients and doctors. Neuropathy is one of those diseases where the mainline, standard treatments seem to have remained static for the last thirty years or more. Occasionally, a different anticonvulsant is tried out, or a combination of antidepressant and anticonvulsant, analgesic, or opiate but this comes more from a feeling of hopefulness than conviction and good science on the part of doctors. In general, people who unfortunately end up with neuropathy from whatever cause (and there are over a hundred!) follow the same medication routes that have been used since the 60’s, until hopefully something works. It really is a sticking a wet finger in the wind sort of medical approach. The downside is that many people are never prescribed anything that really works for them and the symptoms can gradually worsen. In the end, the only pain-killing options are opioids, with all their attendant side effects and addiction potential. Little wonder that all involved tear their hair out with frustration. Medicine isn’t meant to be this way in the 21th Century; even HIV sees progression with its medications!

That’s probably why so many people turn to alternative therapies and supplements to try anything that might relieve the problems. In that sense, different supplements and therapies spring up every year like mushrooms in a field. Some end up being tested and approved and genuinely help people but many are pretty much worthless and a waste of money. That’s the biggest problem with neuropathy; it creates desperation and the need to clutch at straws. Yet the problem is largely unrecognised by the population at large, despite there being 20 million Americans alone who suffer from various forms of nerve damage. To be clear, only certain types of neuropathy can be reversed and even then, only when they are discovered very early in the disease – generally it’s something with you for the long haul.

Over the last decades, it has been a doom and gloom scenario for many people, as they work their way through drugs meant for other diseases in the hope that they will eventually get some relief from their neuropathic symptoms.

However, that very increase in numbers of people suffering serious nerve damage has sparked a wave of studies in the research world and glimmers of hope for sufferers. Unfortunately people living with HIV can’t take any of the credit; if it were just our little demographic, a cynic might suggest that new research wouldn’t be so forthcoming. Luckily for us (but not if you also have diabetes), it is the explosion in diabetes cases that is driving the need for effective treatments for neuropathy. The burgeoning disease of diabetes is the single largest cause of nerve damage, especially in the burger and sugar-guzzling West. That becomes a drain on health budgets and services; ergo a new enthusiasm in the research labs.

The outlook for neuropathy patients may not be quite as gloomy as it once was then and this article will bring you up to date with some of the more recent developments within the scientific and medical world. Be warned though, these will probably not result in ‘cures’ or even off-the-shelf medications in the very near future but do show that the pharmaceutical industry seems to be finally waking up to the fact that this is a huge problem across the entire spectrum of society. Significant progress seems to have been made even during the last year. As you know, drug companies are not known for their philanthropic motives but there’s a vast amount of money to be made as soon as effective treatments can be developed and that, plus pressure from health regulators to deal with diabetes, will unfortunately, probably be the driving force behind finding new treatments. That said; do we care how they get there? Not if we have neuropathy we don’t! Whatever the motives, we’re going to love the pharmaceutical company that brings us genuine relief from nerve damage.
Recent Developments in Research

The following are some of the many recent developments in understanding of how, what and why nerves are damaged and what can be done to alleviate the results.

First, a step backwards but an important one for many people currently being prescribed the anticonvulsant Lyrica (pregabalin) for neuropathy. For those who haven’t already heard, in May 2012 Lyrica (Pregabalin) was dropped as a treatment for diabetic and HIV-related neuropathy by none other than its makers, Pfizer. It proved to be ineffectual in treating neuropathy from those causes. Despite this, doctors all over the world are still prescribing it because they either haven’t heard, or because it’s on the standard list, or they have always prescribed it and have a number of patients for whom it seems to have worked. The fact is that the majority of people have found no improvement from taking Lyrica (pregabalin) and what’s more have suffered more from the side effects than from the neuropathy itself. It may be worth discussing this with your specialist if that’s the case for you. For Pfizer to withdraw support for their own drug is hugely significant – no drug company cuts the throat of its own cash cow for no reason!

By far the largest area of research is at molecular and cellular level which may leave most people scratching their heads and reluctant to read on. However, scientists in both universities and the pharmaceutical company research departments seem to have recently invested a great deal more time in looking at nerve cells, why they are damaged and what processes both chemical and physical cause so much pain and discomfort for neuropathy patients. Of course, this sort of research has undoubtedly been going on for years but with discouraging results, (otherwise new treatments would have been available long before now). The technology must also have improved to the point where more detailed and specific research is now possible. Published scientific findings also stimulate both new research and competition, so exciting results in one university or research lab tend to encourage others to top them with results of their own. More money for research may also be available, as political decisions outside the pharmaceutical industry influence progress. Administrations everywhere are realising the huge costs associated with ‘life-style’ illnesses like, diabetes, cancer, HIV and others. They also realise that continuing to pour money into paying for ineffective treatments with side effects just prolongs the process and increases costs exponentially. The pharmaceutical companies may finally be facing pressure from politicians but they are also beginning to realise the vast profits to be made from finding the ‘mother lode’ of nerve damage treatments. They can no longer really justify making profits from and using up reserves of drugs used for other medical conditions, when they have such a hit and miss effect on neuropathy patients. Sheer numbers and potential profits, then, are driving the search for new drug treatments.

So is it possible to describe some of the developments in molecular and cellular research for nerve damage? I’ll give it a go and have to confess my own understanding is about as shallow as most people’s but we need to have an idea of what sort of treatments are going to affect our futures with this disease. If nothing else, it helps us to understand exactly how complex the whole problem is.

The first is new research that has identified precisely which cells and which sub-sets of cells, are responsible for long-term nerve pain. See an explanation here.

Then studies have identified the cells (Schwann cells) which protect the myelin sheath which is the insulation layer around nerves (to give you an idea, a myelin sheath is like the plastic around electricity wires – you get a short circuit if that is damaged too). More information about this research can be found here.

Further research has identified the importance of something called metabolomics. This looks at why nerve pain persists for so long and why many medications have no effect. The clue lies in a by product of cellular membranes called DMS which seems to be present in large amounts in the spinal cords of lab rats and mice with neuropathy. They are working on finding ways of inhibiting this DMS and thus relieving long-term pain. More information here.

Similarly, American researchers have discovered a group of drug molecules which are found naturally in the body and stabilise other molecules, in order to block neuropathic pain. The idea is that these selective molecules inhibit a key enzyme called soluble epoxide hydrolase. Blocking this enzyme successfully blocks pain sensations. This then has implications for developing new drug treatments which will work much better on neuropathic symptoms. The problem is that the research is still in a very early stage. Read more here.

Another research study aims to block nerve pain signals by using glycene. Glycene is an amino acid which is known as an inhibitory neurotransmitter. It works at the junction between two nerves, known as the synapse and halts the transmission of pain signals along those nerves to the brain. However, glycene quickly dissipates in these places and some have recommended taking supplements to encourage the body to create more naturally. This study questions the efficiency of that but points out that glycene is one of the very promising natural products of the body which needs and is getting much more research. More information here.

Yet another research study has discovered that a certain protein (LRP4) has to be present on the surface of both muscles and in the brain in order to regulate muscle function. If this isn’t the case, several conditions including neuropathy can occur. Many neuropathy patients discover that their muscles stop working efficiently and lose strength after time – the lack of this protein LRP4 in both muscle cells and neurons leads to communication breakdown, which as we all know leads to the numbness, tingling and pain which often appear with nerve damage. Finding a way to either maintain protein levels or introducing it externally may well help reduce the problem. More information here.

Another project has looked into how the brain stores memories of pain and why for instance, phantom limb pain occurs (when a limb is lost, people still feel the pain as if it’s still there). Again, it concerns a type of protein (PKMzeta) which builds and maintains memory by strengthening the connections between neurons. Scientists think that if they can block the activity of PKMzeta, they can reduce the hypersensitivity that causes nerve pain and they’re well on their way to finding something that will do just that. Again, a work in progress we have to say but the future looks a little more hopeful. Read more here.

Finally in this group of studies, the possibilities of nerve transplantation are being explored, in cases where nerves are damaged. This means basically transplanting immature neurons in the hope that they will grow into full nerve cells. During the studies small fractions of the transplanted cells survived and matured into functioning neurons. The cells then integrated into the nerve circuitry of the spinal cord, forming synapses and signalling pathways with neighbouring neurons. Most importantly, as a result, pain hypersensitivity associated with nerve injury was almost completely eliminated. Whether health authorities will be able to cope with the expense of this sort of transplant treatment is the question but there’s little doubt, it sounds promising! More information here.

You can see from these few examples that many people and research labs are busy working at the most basic level of nerve behaviour to find where, why and how, molecular and cellular activity cause such unpleasant neuropathic symptoms. Genetic research is another fast-growing sector, largely due to the huge advancements in techniques in that area and eventually, altered or modified DNA may provide permanent answers. It is slow work though and we have to hope that sooner rather than later a significant breakthrough will be made. Hoping that just one of the studies above may lead to real treatment progress, gives room for optimism.
Researching Nature

Research is not only being done at microscopic levels within the body but studies are also being done in nature to see if there is anything in the animal and plant kingdoms which may help. This has produced some strange studies and conclusions.
A certain sea-snail saliva for instance could be a replacement for morphine in the future. Read more here.
Taiwanese scientists have discovered a compound derived from certain corals called Capnellene. This may also work on certain cells (microglia) and significantly reduce neuropathic pain. More information here.
Scorpion, spider and snake venoms may also provide answers to controlling nerve pain. These venoms work on the sodium channels in the nervous systems of mammals, so it seems logical that controlled doses may help with neuropathic symptoms. Read more here.
Turmeric (also known as Curcumin, Curcuma) which is used widely in cooking, is one of the new buzz words for helping with all sorts of problems including neuropathic pain. Every now and then, a natural remedy emerges that catches on in the market; sometimes with merit and sometimes not. However, one of the most promising is Turmeric or Curcumin, a root used widely in Asian cuisine, generally in powder form. It’s cheap and maybe worth a try – some people swear by it but do your own research. More information here.

Of course the best known natural remedy used to help with neuropathic problems is cannabis. The hysterical reactions to cannabis for medical purposes are much more to do with politics and ‘the war on drugs’ than the medical benefits it can undoubtedly bring for many people. It’s one of the very few recognised effective remedies for neuropathic pain but a) you have to be aware of the laws in your area, b) you have to be able to smoke it (with all its associated lung dangers) and c) you have to be able to cope with getting high (mildly or otherwise). For those reasons many people can’t take advantage of cannabinoids. However, there has been a new synthetic version of THC (the principle working element of cannabis) created by the University of Calgary and this could prove to be a godsend for many neuropathy sufferers because smoking will be removed from the equation. It is far more likely to be accepted by law agencies because it can then be issued on prescription. However, like most developments, we’re not there yet. (Read more here.
Other approaches

There are many more studies and investigations of potential natural remedies, from many different natural sources taking place. If only a handful end up being successful and effective and available to our doctors, or on the shelves of our health food shops, it could relieve suffering for millions.

It seems that no stone is being left unturned in the search for answers and that includes looking at other cultures and other medical practices. Acupuncture and acupressure have been tried by many neuropathy patients over the years, with varying levels of success. Like everything else at the moment, it works for some but not for others. However, new research has discovered that much longer-lasting effects can be achieved by so-called PAP injections (prostatic acid phosphatase) using the same pressure points used for centuries in acupuncture. This so-called PAPupuncture therapy has been proved (in the lab) to extend pain relief much further than with normal acupuncture methods and may well be a useful therapy in the future, for those who don’t wish to increase their drug consumption. Read more here.

Finally in this section, it may seem that the world is turned on its head but a modified version of the herpes virus is thought to theoretically work on peripheral nerves, so that pain can be directly reduced in those areas. A scary thought perhaps, if you’re to be injected with herpes but perhaps logical if you think that Shingles is also a form of neuropathy and is caused by a herpes virus. Anyone suffering from Shingles, knows what nerve pain can do! More information here.

Lastly, apart from the searches for new medications and treatments, which are very difficult for the layman to understand, scientists are also trying to develop better versions of current drug treatments. We know about the random success/failure rate of antidepressants and anticonvulsants and it is likely that there isn’t much progress to be made in those drug areas. We also know about the last resorts in the opioid family. Effective pain killers but often strongly addictive and loaded with side effects, they are unfortunately a question of necessity for many neuropathy patients.

Scientists are discovering that opioids are a group of drugs with more possibilities and their effectiveness is probably more easily adapted and manipulated. Consequently, new opioids and members of the opioid/morphine family are coming on to the market. Tapentadol,(Nucynta in the USA and Palexia in Europe) for instance, is newly approved in the States and can be equated to Tramadol but works slightly differently, more effectively and with less side effects. It will be a welcome alternative for many people. Read more here.

Researchers are also looking for ways to prolong the pain-killing effects of morphines and opioids, thus reducing the need for higher doses and reducing addiction dangers. They have found that Resveratrol, (naturally found in red wine) can preserve the effects of morphine in rats - most importantly, in rats that have developed morphine tolerance. In humans, morphine tolerance creates a need for higher doses to achieve the same effect so discovering something that delays tolerance, or maintains the pain killing effects, is clearly of great value. See more here.
Conclusion

If you’ve got this far, you’re probably reeling from information-overload but the intention is to reassure you that serious efforts are being made to find solutions for both nerve damage and the uncomfortable results of that for millions of people. Eventually, a few will make it through the rigorous processes and end up as viable options for our doctors to prescribe. Unfortunately, it takes time and that’s difficult to swallow for a patient in extreme pain or discomfort. You’re already on drugs for your neuropathy; they may be working or not, or just partly. All you want is something to take the problem away and preferably a one-drug-cures-all type of treatment. The truth is that that’s not going to happen in the very near future but it will eventually happen. Finally, health authorities and pharmaceutical companies are getting their acts together and working for us instead of palming us off with dangerous drugs meant for other diseases.

Money will play a part in the speed of progress and research finance is often the first to go in times of financial crisis, along with the willingness of health authorities and insurance companies to pay for expensive new drugs but the picture is brighter than ten years ago. All concerned are realising that neuropathic pain is a far greater problem than they ever imagined and the increase of the diseases that cause it (along with people living longer) is only going to make that bigger. Something has to be done to reduce the costs of long term treatment and that means finding things that genuinely work. Lab rats and mice may view this with horror but for many people with neuropathy, it just can’t come soon enough!

http://www.positivelite.com/component/zoo/item/neuropathy-and-hiv-a-progress-report

FIRST WHO REPORT ON SUICIDE PREVENTION

More than 800 000 people die by suicide every year – around one person every 40 seconds, according to WHO's first global report on suicide prevention, published today. Some 75% of suicides occur in low- and middle-income countries.

Pesticide poisoning, hanging and firearms are among the most common methods of suicide globally. Evidence from Australia, Canada, Japan, New Zealand, the United States and a number of European countries reveals that limiting access to these means can help prevent people dying by suicide. Another key to reducing deaths by suicide is a commitment by national governments to the establishment and implementation of a coordinated plan of action. Currently, only 28 countries are known to have national suicide prevention strategies.

Suicide is a global phenomenon

Suicide occurs all over the world and can take place at almost any age. Globally, suicide rates are highest in people aged 70 years and over. In some countries, however, the highest rates are found among the young. Notably, suicide is the second leading cause of death in 15-29 year-olds globally.

“This report is a call for action to address a large public health problem which has been shrouded in taboo for far too long” said Dr Margaret Chan, Director-General of WHO.

Generally, more men die by suicide than women. In richer countries, three times as many men die by suicide than women. Men aged 50 years and over are particularly vulnerable.

In low- and middle-income countries, young adults and elderly women have higher rates of suicide than their counterparts in high-income countries. Women over 70 years old are more than twice as likely to die by suicide than women aged 15-29 years.

Suicides are preventable

Reducing access to means of suicide is one way to reduce deaths. Other effective measures include responsible reporting of suicide in the media, such as avoiding language that sensationalizes suicide and avoiding explicit description of methods used, and early identification and management of mental and substance use disorders in communities and by health workers in particular.

Follow-up care by health workers through regular contact, including by phone or home visits, for people who have attempted suicide, together with provision of community support, are essential, because people who have already attempted suicide are at the greatest risk of trying again.

 “No matter where a country currently stands in suicide prevention”, said Dr Alexandra Fleischmann, Scientist in the Department of Mental Health and Substance Abuse at WHO, “effective measures can be taken, even just starting at local level and on a small-scale”.

WHO recommends countries involve a range of government departments in developing a comprehensive coordinated response. High-level commitment is needed not just within the health sector, but also within education, employment, social welfare and judicial departments.

“This report, the first WHO publication of its kind, presents a comprehensive overview of suicide, suicide attempts and successful suicide prevention efforts worldwide. We know what works. Now is the time to act,” said Dr Shekhar Saxena, Director of the Department of Mental Health and Substance Abuse at WHO.

The report’s launch comes just a week before World Suicide Prevention Day, observed on 10 September every year. The Day provides an opportunity for joint action to raise awareness about suicide and suicide prevention around the world.

Working towards a global target

In the WHO Mental Health Action Plan 2013-2020, WHO Member States have committed themselves to work towards the global target of reducing the suicide rate in countries by 10% by 2020. WHO’s Mental Health Gap Action Programme, launched in 2008, includes suicide prevention as a priority and provides evidence-based technical guidance to expand service provision in countries.