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THERAPEUTIC VALUE OF NALTREXONE AS A GLIAL MODULATOR
Session: MP-08a
Fri, Nov. 17, 4:45-6:45 pm
Hampton Room

Please note, medically challenging cases are removed three months after the meeting and scientific abstracts after three years.

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THERAPEUTIC VALUE OF NALTREXONE AS A GLIAL MODULATOR
D. Agarwal1, K. Toljan2, H. Qureshi1, B. Vrooman3
1
Cleveland Clinic, Anesthesiology, Cleveland, United States
2 School of Medicine, University of Zagreb, Zagreb, Croatia
3Cleveland Clinic, Pain Management, Cleveland, United States

 

Introduction:

 

  Naltrexone, a traditional mu-opioid receptor (MOR) antagonist, has recently been used for treating autoimmune related pain syndromes in a dosing range 1.5 – 4.5 mg per day.1 This is a tenth of the traditionally prescribed MOR antagonist dose and has been dubbed low-dose naltrexone (LDN). Current evidence demonstrates that naltrexone exhibits three qualitatively distinct effects in relation to the drug concentration. In nanogram and microgram doses, also called ultra low-dose naltrexone, analgesic effects of opioid are potentiated via modulation of MOR second messaging.2 As low dose, LDN acts via Toll-like receptor 4 on microglial cells and attenuates neuroinflammation.1,3  And in classical milligram dosing, naltrexone dosing elicits opioid antagonism.

 

Fig 1.

 

Fig 2.

 

  The multiphasic dose-effect curve of the aforementioned compounds is in concordance with principles of hormesis. A non-linear dose-effect curve demonstrates that naltrexone may be considered a hormetin. Translating the knowledge from basic pharmacological studies to clinical setting points to LDN and ultra LDN as being valid modalities for treating pain. This study is meant to explore the clinical uses of LDN, patient outcomes with LDN treatment, and to determine a standardized treatment regimen.

 

Table 1

 

Materials and Methods.

 

A single center, retrospective study was conducted on a cohort of patients. All patients were prescribed LDN from 2013 to 2017 in an outpatient chronic pain clinic. Pain scores were measured on a universal 0-10 verbal pain assessment tool. Inclusion criteria for study included diagnosis of an autoimmune chronic pain condition (Including chronic regional pain syndrome (CRPS), multiple sclerosis (MS), and Fibromyalgia), and being prescribed LDN and having at least 1 data point of outpatient clinic follow up after initial meeting. Exclusion criteria for the study included not having an outpatient clinic follow up, not having a diagnosed chronic pain condition. Of 110 patients eligible for the study, 41 met all criteria and did not have any gaps in their data.

 

Results:

 

  Our clinical data from a heterogenic group of 41 out of 110 patients treated with LDN showed that 22 had improvement in pain, while 19 did not have an improvement in their pain scores. Patients displaying improvement in symptoms had an average pain score decrease of 0.95, while those who did not showed a 0.16 point increase in their pain score. Common pain diagnoses included neuropathic and myofascial pain conditions with a likely autoimmune etiology, frequently refractory to other medications. Patients were prescribed compounded LDN at doses between 1 and 4.5mg/day, with the most common formulation being 1.5mg nightly, increased to 3mg qhs after 2 weeks if necessary. Substantial benefits in terms of pain reduction and occasional primary condition regression were noted. Notably, decreased pain was reported in patients diagnosed with CRPS (13/21), multiple sclerosis (4/5) and fibromyalgia (8/9), the latter group also noting lower rate of flare-ups. Side effects were rarely occurring, primarily as headache and nausea. Patients were required to be off of opioid medication prior to taking LDN. Due to missing patient data, a detailed analysis of patients with RSD could not be completed.

 

Table 2

 

Discussion.

 

LDN has been primarily used as a treatment for pain related to fibromyalgia, complex regional pain syndrome and inflammatory bowel disease.1 Our data shows that there is self reported improvement in both pain and disease-specific ailments in patients with fibromyalgia, CRPS, and multiple sclerosis. Specific examples range from feeling less “tired” to having fewer multiple sclerosis “flares”. While subjective and non-randomized, this data offers a promising direction for further research into glial modification properties of LDN.

 

Directions for future research include, establishing an evidence-based dosing regimen and searching for the optimum dose range, finding true indications and contraindications for LDN as a treatment, and determining the safety profile of LDN and potential adverse effects.

 

REFERENCES

 

1. Younger J, Parkitny L, McLain D. The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic pain. Clin Rheumatol. 2014;33(4):451-9.

2. Burns HL, Wang HJ. Ultra-Low-Dose Naloxone or Naltrexone to Improve Opioid Analgesia: The History, the Mystery and a Novel Approach. Clinical Medicine Insights: Therapeutics 2010;2:857-868.

3. Wang X, Zhang Y, Peng Y et al. Pharmacological characterization of the opioid inactive isomers (+)-naltrexone and (+)-naloxone as antagonists of toll-like receptor 4. Br J Pharmacol. 2016;173 (5):856-69. 

 

 

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