Bisphosphonate – Pamidronate – Safety Summary – For Serious Pain from CRPS

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Bisphosphonates for Complex Regional Pain Syndrome?

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If you have Complex Regional Pain Syndrome and you have severe pain that has failed all remedies, you may wish to consider bisphosphonate infusions for pain relief. This area needs more research – there is almost none, only three or four small publications on pamidronate for chronic noncancer pain that I posted here.

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Those posts on bisphosphonates in the last two weeks have developed the background to the use of bisphonates for chronic noncancer pain. This is not everyday medicine for pain control, but it is common for certain cancers and for osteoporosis.

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There is a science behind this choice. There is a strong rationale, it makes sense, but this is serious therapy.

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We do not know if it will work or how many may benefit.

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To my knowledge, it has not been done outside of those three or four very small studies. No one is offering this therapy for CRPS. But we all see patients who have tried and failed every known therapy that exists, and pain has taken their lives.

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Here we review these specific points:

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-Safety

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-How soon you can consider pregnancy after treatment?

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-Side effects with the infusion

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-Calcium supplements you need to take

 

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Information has been taken from the award winning website of Susan Ott, Professor of Medicine at University of Washington and an expert on bisphosphonates and metabolic bone disease. Her teaching goes beyond what can be gleaned from publications, and thankfully spans the depth of the field. It is a concise encyclopedia of bisphosphonates for physicians and patients. Apologies to Professor Ott, I have quoted her work liberally.

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SAFETY

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Safety issues are discussed in this editorial Long Term Safety of Bisphosphonates by Professor Ott.

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“Unlike most medications, bisphosphonates remain in the body for decades. These drugs are not metabolized….The amount of drug within the bone will accumulate with use. There is no known method of removing the medication from the bones. The duration of physiological effect is still unknown.”

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Further, she notes the reduced risk of fracture is not closely linked to the increase in bone density. Fracture rate was higher with increased density. E.g., hip fracture decreased with 2.5 mg/d risedronate relative to placebo, but 5.0 mg/d was same as placebo.

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The issue:

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As bone mineralization increases, bone becomes more brittle.

Brittle bone may be more susceptible to fracture.

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PREGNANCY

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It is recommended that you not become pregnant while bisphosphonate is in your bones.

It is contraindicated in women who are pregnant or planning pregnancy.

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Her advice: wait at least one year after stopping the medication to try getting pregnant. The drugs are still excreted in the urine 8 years after stopping.

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Women who are pregnant should not take bisphosphonates. If women are already taking a bisphosphonate and want to become pregnant, it is not clear how long they should wait [my emphasis]. Until more information is available, I suggest waiting at least one year after stopping the medication to try getting pregnant. If a woman is taking a bisphosphonate and inadvertantly gets pregnant and wants to continue the pregnancy, she should be carefully followed, with measurements of calcium and optimal vitamin D levels. Calcitonin is a safe drug to use during pregnancy if bone loss is a concern.

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See below, for more details on toxicity studies in pregnancy.

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SIDE EFFECTS AFTER THE INFUSION

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The day after the infusion it is common to have a fever. Some patients feel like they are getting the flu and feel aching and tired. This usually lasts only one or two days. You may have pain in the bone, especially if you have Paget’s disease or fibrous dysplasia. Other complications are not common, and include a transient decrease in the white blood cell count or blood calcium. The infusion site may become sore or infected. Rare side effects are inflammation of the eyes, kidney damage, or problems with the bones underneath the teeth.

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To be safe, the following blood tests should be normal before giving pamidronate: calcium (greater than 9.0 mg/dl) creatinine, white blood cell count, vitamin D (at least 20 ng/ml). It should not be given during an active infection.

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More detailed studies of blood that I do will also include post infusion study of urine for urinary cross-linked N-terminal telopeptides of type I collagen (NTX).

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CALCIUM SUPPLEMENTS – WHICH ONES?

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Patients need to be sure to get adequate calcium and vitamin D after pamidronate infusions.

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Professor Ott recommends specific calcium supplements — not all are equal. “Many brands do not dissolve in the intestines, so the calcium is not absorbed into the bloodstream.”

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She lists these brands to take, with photos and cost in order of price:

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TUMS EX – least expensive, Caltrate, Oscal, Viactiv, Citracal – most expensive

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Calcium carbonate should be taken with food. Calcium citrate can be taken on empty stomach. Take twice daily. Do not get calcium with magnesium – magnesium may compete with calcium, i.e. block it.

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TOXICITY STUDIES

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Effects of bisphosphonates during pregnancy. Bisphosphonates should be avoided during pregnancy. Refer to her summary for details of animal toxicity studies and human studies.

 

Here is a copy of the 2004 FDA label information for pamidronate:
Pregnancy Category D (See WARNINGS)

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There are no adequate and well-controlled studies in pregnant women.
Bolus intravenous studies conducted in rats and rabbits determined that Aredia produces maternal toxicity and embryo/fetal effects when given during organogenesis at doses of 0.6 to 8.3 times the highest recommended human dose for a single intravenous infusion. As it has been shown that Aredia can cross the placenta in rats and has produced marked maternal and nonteratogenic embryo/fetal effects in rats and rabbits, it should not be given to women during pregnancy.

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Bisphosphonates are incorporated into the bone matrix, from where they are gradually released over periods of weeks to years. The extent of bisphosphonate incorporation into adult bone, and hence, the amount available for release back into the systemic circulation, is directly related to the total dose and duration of bisphosphonate use. Although there are no data on fetal risk in humans, bisphosphonates do cause fetal harm in animals, and animal data suggest that uptake of bisphosphonates into fetal bone is greater than into maternal bone. Therefore, there is a theoretical risk of fetal harm (e.g., skeletal and other abnormalities) if a woman becomes pregnant after completing a course of bisphosphonate therapy. The impact of variables such as time between cessation of bisphosphonate therapy to conception, the particular bisphosphonate used, and the route of administration (intravenous versus oral) on this risk has not been established.

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Nursing Mothers
It is not known whether Aredia is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Aredia is administered to a nursing woman.

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The material on this site is for informational purposes only, and is not a substitute for

medical advice, diagnosis or treatment provided by a qualified health care provider.

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Please understand that it is not legal for me to give medical advice without a consultation.

If you wish an appointment, please telephone my office.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Bisphosphonates in Treatment of Complex Regional Pain Syndrome, continued

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A new publication out of Germany, May 2014, in the journal Pain, suggests a strong rationale for the use of bisphosphonates in the treatment of Complex Regional Pain Syndrome (CRPS).  See my review of those infusions..\

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Impaired bone metabolism is a feature of CRPS.

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They found evidence that osteoprotegerin (OPG) was elevated in serum of persons with CRPS. That is not unique to CRPS, but it might be useful as a potential biomarker for CRPS. It is also increased with osteoporosis, coronary heart failure, irritable bowel syndrome, and is it associated with long term renal dysfunction.

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OPG is an inhibitor of osteoclast formation, important for bone remodeling and it may contribute to CRPS pathophysiology.

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They compared OPG with triple phase bone scan (TPBS).

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For the CRPS-affected hand, a significant correlation between OPG and TPBS region of interest analysis in phase III was detected. The persistent OPG increase in CRPS indicates enhanced osteoblastic activity shown by increased radiotracer uptake in TPBS phase III. A contribution of bone turnover to CRPS pathophysiology is likely. OPG might be useful as a biomarker for CRPS.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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This site is not email. If you wish an appointment, please telephone the office to schedule.

It is not legal for me to provide medical advice without an examination.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

 

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Bisphosphonates for Pain – Back Pain, CRPS Pain. Have You Received Pamidronate or Other IV Bisphosphonate for Pain?

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Bisphosphonates have been used for treatment of pain.

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I have reviewed a few studies on pamidronate infusions for pain,  below.

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Based on these small studies, there is a growing rationale for use of I.V. pamidronate in the setting of selected chronic intractable pain syndromes.

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Have you received IV Pamidronate or Reclast or any bisphosphonate

for treatment of pain caused by any condition?

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Bisphosphonates are effective for reducing bone loss and, separate from that mechanism, they have been used to reduce pain in persons with various conditions including Complex Regional Pain Syndrome, ankylosing spondylitis, rheumatoid arthritis, chronic back pain, and other conditions.

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After you vote, if you wish to see results, click on the words “View results.” You do not need to sign in or give your email. Simply view results.

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If you have any experience with bisphosphonates even if for osteoporosis, please comment below. Do you know which academic centers are giving IV bisphosphonates for pain?

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The mechanism of pain relief is not clear and there are no standardized protocols for the use of bisphosphonates for pain, but relief of pain is believed to be separate from mechanisms related to bone.

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Many patients have no other options for treatment. There are no large randomized controlled studies – where is NIH funding for pain?

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Many medical treatments do not work for some patients with Complex Regional Pain Syndrome or for chronic low back pain. When all else has failed, pamidronate may be given IV, often in a series of infusions that take up to four hours. There may be some flu-like symptoms for 1 to 3 days after.

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For reasons unknown to us, Complex Regional Pain Syndrome is often associated with bone loss in the area of pain. It is more marked and prolonged than in immobilized trauma patients.

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What dose should be used, how often should it be given? Few studies have been published.

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MEDICATIONS for OSTEOPOROSIS

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Bisphosphonate therapy is commonly used for diseases of bone such as osteoporosis or Paget’s Disease, multiple myeloma, bone metastasis, osteogenesis imperfecta, fibrous dysplasia. For example alendronate (Fosamax) or residronate (Actonel) tablets,  pamidronate infusions,  or others.  Zoledronic acid (Reclast) is given IV, usually only once each year. One form of ibandronate (Boniva) is also given IV, usually every 3 months.

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Other medications that are not bisphosphonates are used for osteoporosis such as calcitonin-salmon (Miacalcin) SC or IM injections, Forteo (rhPTH ) SC injections, or estrogen.

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MECHANISM of BISPHOSPHONATES

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Bisphosphonates slow the rate of bone loss, they do not actually build bone. Bone requires a balance of osteoblasts that form new bone, and osteoclasts that resorb bone. Osteoporosis occurs with age and especially with loss of estrogen that dramatically increases loss of bone. Other factors that lead to bone loss are lack of exercise, hormonal, nutritional and genetic predispositions.

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RISKS of OSTEOPOROSIS

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Some of the worst pain I have seen in my career is pain due to fractures of fragile osteoporotic bones. It may be impossible to treat. With osteoporosis, you may simply roll over in bed and 7 rib fractures occur. One woman developed hundreds of fractures throughout her pelvis and was bedridden for years after a very minor incident. Bone stimulators did not help and she could not walk or stand without help. Years later there was a 1-1/2 inch gap between the fractures in her pelvis and of course being inactive and bedridden can only make osteoporosis worse.

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RISK of MEDICATION for OSTEOPOROSIS

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Osteoporosis is more dangerous by far than any medication used to treat it. As with any drug, the benefit must outweigh side effects. Bisphosphonates increase bone thickness and reduce risk of fractures. Osteoporosis medications causes less than 1% risk of bone fractures. Fractures from the medications may be seen in the midshaft of the femur which is the mid thigh; and they may cause osteonecrosis of the TMJ, the jaw bone. Serious problems with bone healing after dental surgery may occur in those who take bisphosphonates. But the risk of osteoporosis is far greater than this small risk.

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Non-bisphosphonates also have dangers: Calcitonin may increase risk of cancer. PTH is the only one that can actually build bone – an anabolic agent that induces bone formation, not just prevent resorption of bone, but abrupt termination leads to rapid loss of bone density. Estrogen increases risk of clotting, thromboembolism that is a risk for stroke.

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Neridronate is a new bisphosphonate available so far only in Europe the last few years. They are making claims that a series of neridronate infusions can reduce pain 100% in persons with Complex Regional Pain Syndrome. That seems highly unlikely:  100% effective? Really? Oh, and so far no reports of necrosis of bone. But it has not been available as long as pamidronate, so it may be years before we get a better assessment of this drug that is confirmed by other laboratories.

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PUBLICATIONS

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Dr. Pappagallo published three of the studies below. He is one of the foremost scientist-pain specialists in the world.

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A pilot trial of intravenous pamidronate for chronic low back pain

PAIN, Volume 155, Issue 1 , Pages 108-117, January 2014,  Pappagallo et al, found no serious adverse events.

They tested four groups of 11 subjects (7 active, 4 placebo) at differing doses. They conclude:

i.v. pamidronate, administered as two 90 mg infusions four weeks apart, decreased pain intensity for 6 months in subjects with CLBP.

[Pain was decreased by > 4 points. They showed no relationship between bone density and analgesic response, but did find a relationship between PTH, vitamin D status and pain response.]

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Bisphosphonates are known to have significant analgesic activity in addition to their well-characterized role in inhibiting bone resorption. For example, pamidronate (Aredia®, Novartis), an aminobisphosphonate, demonstrates clinically significant pain relief when administered intravenously for the treatment of Paget’s disease, metastatic breast cancer and osteolytic lesions of multiple myeloma [5], [24], [51]. In addition, i.v. pamidronate has been shown to have analgesic activity in a wide variety of painful conditions, including complex regional pain syndrome [12], [44], [53], fibrous dysplasia [10], recurrent multifocal osteomyelitis [22], [35], ankylosing spondylitis [33], rheumatoid arthritis [31], and others (for review, see [49]). The mechanism(s) of this analgesic effect is not fully known, but antinociceptive effects of pamidronate and other bisphosphonates have been reported in animal models of pain [7], [8], [25], [52]. Inhibition of osteoclast proton secretion and other cellular and molecular mechanisms may contribute to the analgesic effect [37], [54].

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The molecular mechanisms of pamidronate’s analgesic effects are not fully understood. Bisphosphonates are known to inhibit the activity and/or cause apoptosis of osteoclasts [20], [46], which remodel bone by creating an acidic microenvironment via the release of protons through vacuolar H+-ATPase [6], [45]. Osteoclast-induced high concentrations of protons may activate acid-sensing ion channels and transient receptor potential vanilloid type 1 channels expressed by small nerve fibers involved in pain signal transmission [37], [42], [54]. Osteoclasts appear to have a role in inflammatory pain adjacent to bone and in the hyperalgesia observed in type IX collagen-deficient mice [2], [37]. Of interest, inhibition of osteoclasts by bisphosphonates in a rat model of degenerative joint disease has recently been found to prevent subchondral bone resorption and cartilage loss, and decrease pain [50]. Clinical findings may also suggest a role for subchondral bone changes in the early development of painful osteoarthritis [13], [36]. Furthermore, the anatomical core structure of the spine is made of bone tissue, and immunohistochemical studies have revealed the presence of a widespread network of peptidergic small sensory fibers throughout the bone marrow, mineralized bone, and periosteum [28], [32]. Thus it is conceivable that: a) nonspecific low back pain (associated with degenerative disk disease or spondylotic disease as in our study population) may be related to sensitization of bone nociceptors, plausibly in the context of subchondral bone resorption (eg, at the vertebral endplates and/or facet joints) and b) inhibition of subchondral osteoclasts (and possibly of other phagocytic or inflammatory bone resident cells) by i.v. pamidronate might be clinically relevant to the treatment of CLBP.

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The responder rate for pamidronate 180 mg increased from 50% at 24 hours after the second infusion to 100% at month 2; the 100% responder rate was maintained at all subsequent time points. [There were 7 patients in each group of this small study.]

(Fig. 3) illustrates that all subjects receiving 180 mg pamidronate had at least 50% pain relief at both 3 and 6 months postinfusion, and approximately 80% of subjects receiving 180 mg pamidronate had 100% pain relief at 6 months.

Fig. 3. Continuous responder analysis. Blue solid line, placebo; red dashed line, 30 mg pamidronate; green dashed/dotted line, 60 mg pamidronate; brown dashed line, 90 mg pamidronate; purple dashed/dotted line, 180 mg pamidronate.

 

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Pamidronate treatment in rheumatology practice: a comprehensive review

Clinical Rheumatology, Volume 28, Issue 12, pp 1359-1364, December 2009, Slobodin et al. from Israel.

The efficacy of pamidronate in patients with spondyloarthropathies; synovitis, acne, pustulosis, hyperostosis, and osteitis syndrome; hypertrophic osteoarthropathy; osteoporotic vertebral fractures; chronic back pain due to disk disease or spinal stenosis; Charcot arthropathy; transient osteoporosis; and complex regional pain syndrome-I, has been demonstrated in more than 40 reports, the majority of which, however, were not controlled studies. In some of reviewed conditions, aside from providing analgesic relief, pamidronate may also have disease-modifying properties. While used in different doses in a variety of rheumatic disorders, pamidronate was generally reported to be well tolerated with an overall good safety profile. Pamidronate may represent an effective and safe choice for a spectrum of rheumatic patients, suffering from intractable musculoskeletal pain, unresponsive to traditionally recommended therapies. Large randomized, controlled studies examining the efficacy of pamidronate in the rheumatic conditions are urgently needed.

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Complex regional pain syndrome (CRPS/RSD) and neuropathic pain: role of intravenous bisphosphonates as analgesics. ScientificWorldJournal. 2008;8:229–236Yanow J, Pappagallo M, Pillai L.  They review multiple studies for pain of CRPS.

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Efficacy of pamidronate in complex regional pain syndrome type I. Pain Med. 2004;5:276–280, Robinson JN, Sandom J, Chapman PT from New Zealand.

Pamidronate 60 mg iv was given only one time to 14 patients, 13 placebo controls.

Overall improvements in pain score, patient’s global assessment of disease severity score, and physical function (SF-36) score were noted in the pamidronate group at 3 months, and improvements in role physical (SF-36) score were noted at 1 and 3 months. There was variability in pamidronate response among individuals. CONCLUSIONS: Pamidronate may be a useful treatment option in the management of patients with CRPS Type I. Although treatment response was variable, the majority of patients improved.

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Treatment of chronic mechanical spinal pain with intravenous pamidronate: a review of medical records. J Pain Symptom Manage. 2003;26:678–683, Pappagallo M, Breuer B, Schneider A, Sperber K.

[They] reviewed the charts of 25 patients who had experienced disabling spinal pain for several years, and whom we treated with [iv] pamidronate. None had a history of osteoporotic vertebral fractures or metastatic disease. Pain rating scores decreased in 91% of patients: on a 0–10 numeric rating scale, the mean pain change was 3.6 points and mean percentage change was 41% (P <0.0001).

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Treatment of severe, recalcitrant reflex sympathetic dystrophy: assessment of efficacy and safety of the second generation bisphosphonate pamidronate. Clin Rheumatol. 1997;16:51–56, Cortet B, et al. from France infused 14 patients 1 to 3 days, followed 3 months and in one case for 9 months. “results suggest an efficacy” and they recommended double blind placebo controlled studies.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Please understand that it is illegal for me to give medical advice

without seeing you in office for history and examination.

I cannot respond to your medical questions unless you schedule an evaluation.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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PEA Palmitoylethanolamide – “Glia & Mast Cells as Target, An Anti-Inflammatory & Neuroprotective Lipid Mediator”

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Another oustanding article on palmitoylethanolamide “PEA.” I have seen profound results with it relieving intractable neuropathic pain in a woman with CRPS for years, and I suspect it may help Major Depressive Disorder but that remains to be tested.

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I need to add that opioids create pain. One mechanism by which that occurs is that opioids create pro-inflammatory cytokines, which creates more pain. Patients may see no response to essential pain relieving medications untill they taper off all opioids and allow the system to stabilize. Otherwise, they will have pain forever and it may increase.

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Glia and mast cells as targets for palmitoylethanolamide,

an anti-inflammatory and neuroprotective lipid mediator

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Authors  Skaper SD, Facci L, Giusti P.

Mol Neurobiol. 2013 Oct;48(2):340-52.  Epub 2013 Jun 28.

Abstract

Glia are key players in a number of nervous system disorders. Besides releasing glial and neuronal signaling molecules directed to cellular homeostasis, glia respond also to pro-inflammatory signals released from immune-related cells, with the mast cell being of particular interest. A proposed mast cell-glia communication may open new perspectives for designing therapies to target neuroinflammation by differentially modulating activation of non-neuronal cells normally controlling neuronal sensitization-both peripherally and centrally. Mast cells and glia possess endogenous homeostatic mechanisms/molecules that can be upregulated as a result of tissue damage or stimulation of inflammatory responses. Such molecules include the N-acylethanolamines, whose principal family members are the endocannabinoid N-arachidonoylethanolamine (anandamide), and its congeners N-stearoylethanolamine, N-oleoylethanolamine, and N-palmitoylethanolamine (PEA). A key role of PEA may be to maintain cellular homeostasis when faced with external stressors provoking, for example, inflammation: PEA is produced and hydrolyzed by microglia, it downmodulates mast cell activation, it increases in glutamate-treated neocortical neurons ex vivo and in injured cortex, and PEA levels increase in the spinal cord of mice with chronic relapsing experimental allergic encephalomyelitis. Applied exogenously, PEA has proven efficacious in mast cell-mediated experimental models of acute and neurogenic inflammation. This fatty acid amide possesses also neuroprotective effects, for example, in a model of spinal cord trauma, in a delayed post-glutamate paradigm of excitotoxic death, and against amyloid β-peptide-induced learning and memory impairment in mice. These actions may be mediated by PEA acting through “receptor pleiotropism,” i.e., both direct and indirect interactions of PEA with different receptor targets, e.g., cannabinoid CB2 and peroxisome proliferator-activated receptor-alpha.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Complex Regional Pain Syndrome – Review of Inflammation & Meta-analysis

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Neurology, the journal of the Academy of Neurology, has published “Inflammation in Complex Regional Pain Syndrome, a systematic review and meta-analysis” on July 1, 2013.

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The study was supported by grants from the Australian National Health and Medical Research Council, the Canadian Institute of Health Research, the Dutch consortium on CRPS and the Dutch Ministry of Economic Affairs.

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They found “a proinflammatory state in blood, blister fluid, and CSF.” Profiles differed in acute and chronic cases.

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Levels of neuropeptides in blood and blister fluids were not higher in CRPS than in controls.

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The inflammatory profile reflected a generic chronic pain state. There was no signature specific to CRPS. Chronic pain is associated with higher levels of proinflammatory activity.

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Acute cases did differ from chronic. But affected limbs did not show higher levels of inflammation than limbs that were not affected.

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Of interest, they found significant variability in concentrations of inflammatory factors which may suggest the data reflects methodological errors. Or it may suggest that CRPS is not a distinct disorder but is a collection of disorders that appear similar clinically, or the inflammatory response is not consistent, or that important clinical subgroups exist, for example hot vs cold CRPS or variations that present with significant autonomic disorders or systemic involvement.

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They noted a recent review of treatments that found little evidence that prednisolone improves symptoms of CRPS. And they note conflicting evidence for free-radical scavengers (dimethyl sulfoxide and N-acetylcysteine). They point out the latter trials were small and of mixed quality, however I have personally seen patients who respond to those treatments.

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They recommended formal, large, high quality studies to assess the efficacy of cytokine inhibitors (TNFα inhibitors) or immunosuppressive medication. They recommended more in vivo work on the immunomodulatory effects of analgesic medications such as morphine that has, in vitro, been shown to decrease the anti-inflammatory cytokine IL-10 and increase the proinflammatory IL-12 thus predisposing to more pain.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~~~~

Please understand that it is not legal for me

to give medical advice without a consultation.

If you wish an appointment, please telephone my office.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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LDN – Low Dose Naltrexone – Prescribing Doctor Videos

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Prescribing Doctor Videos

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The low dose naltrexone, LDN, website is managed by volunteers in England, in particular Linda Elsegood, Trustee. All the videos are no doubt helpful, but I would point out particular interviews:

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Rachel Allen, PhD – England – Dr. Allen received her PhD in Immunology from Oxford, then did work in Cambridge on the innate immune system.  She discusses the innate and adaptive immune system, glia, cytokines, and dendritic cells. This video focuses on Toll-Like Receptors which is where naltrexone acts to block pro-inflammatory cytokines that create pain. The pro-inflammatory cytokines are involved in autoimmune and other diseases.

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Jarred Younger, PhD – Stanford researcher  – has published studies using LDN on persons with fibromyalgia.  He discusses plans for testing it on other conditions possibly including depression and using it for children.

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Pradeep Chopra, MD – Anesthesiologist in Rhode Island – uses LDN for CRPS. With Mark Cooper, PhD, they have published two cases. The publication acknowledges my contribution in teaching them my experience. I have prescribed LDN for years in many persons with intractable pain. Prof. Cooper came to San Diego for two days November 2011, to meet and interview eight of my patients who had 100% responses with LDN for their years of intractable pain. Four responders had been able to discontinue LDN with no further recurrence of pain for years, and four remained on LDN with complete response.

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Since I had no time to publish, Dr. Cooper later asked that I teach Dr. Chopra about LDN which I did over several hours. After noting in the paper that Dr. Chopra’s patient did not fully respond, I suggested to Dr. Chopra that he increase the dosage as I find not all respond to 4.5 mg. A large percentage of persons with intractable pain need higher doses. Finally, there are two populations that need lower doses than 4.5 mg but most persons with pain can be started at that dose.

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The material on this site is for informational purposes only.

It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~~~~

Please understand that it is not legal for me

to give medical advice without a consultation.

If you wish an appointment, please telephone my office.

.

For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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