All that I have been reading about low dose naltrexone seems to good to be true. Anybody know anything this drug?

I've been taking LDN for about 2 1/2 months, along with several other treatments. I don't know if it is what is preventing my symptoms from progressing, but I wouldn't want to give it up. Supposedly, it is more effective for MS than for PD, but I have seen ancedotal accounts of how it can stop PD progression, and that's good enough for me. It's cheap, too, so it's not a financial burden.

Tom Thanks for the info- LR

hi little rock and welcome.

we have many posts about ldn on neurotalk.

use the search feature located up toponthe blue tool bar.

most will be on the ms forum, but there were some thread recently here on pd.

LDN is not a cure..It supposedly arrests the progression of pd..All I can say about it is that we have a member who is taken it, and has not progressed in about 47 months

I have been taking a half teaspoon of cough syrup with Dextromethorphan before bedtime for about 15 months, which according to a study conducted by Dr Hong in pd induced rats, is supposed to do the same thing..I did exceptionally well for about 11 months, but I find now that I am becoming more symptomatic, and I know that I am due for another med increase..I am still doing realitively well however considering Im into my sixth year with pd

Robert, is another member who is also taking DM and he has not progressed much since he began the regimen..Im sure he and AshleyK will weigh in with their experiences..Ashley is taking LDN

are doing so on the strength of work done by Dr. J.S. Hong in which he demonstrated in animal studies that it is as effective as naltrexone in preventing the inflammation response of microglial cells thought to be the culprit in damaging dopamine-producing brain cells. Although naltrexone is relatively inexpensive, it does require a physicians's prescription, and the cough preparations containing DM do not.
Like Steve said, the claims made for naltrexone, even for MS, are that it appears to stop progression of the disease. I assume that the effectiveness we think we have seen with low-dose DM in PD is slowing of disease progression, not a cure.
My progression has been slow, as indicated by very little loss of normal gait, and fairly well-sustained stamina during the five years I have been using DM. I have required only small increases in meds (sinemet and amantadine, supplemented with CoQ10) over that time, and my neurologist is extremely happy with my history so far.
Bear in mind that I was in the earliest stages of PD when diagnosed in 2001, and may still be in what some have called the "honeymoon" period of responsiveness to sinemet.

Below is a recent ABC News video on LDN from the Low Dose Naltrexone website. The LDN website believes that low doses of naltrexone increase endorphins in the brain thus enhancing the immune system. There do not seem to be any valid tests done in humans yet to show this to be true. Although, a recent clinical trial done in Milan with MS patients and LDN has yet to be made public so maybe that will settle the matter. I think the work done by Dr. Hong, Head of the Pharmacology Group of the NIH shows more convincing reasons on how LDN seems to work. They have produced many papers over the past eight years showing that opioid receptor antagonists like LDN and dextromethorphan, DM, can greatly reduce neuro-inflammation in PD induced rodents.
http://www.lowdosenaltrexone.org/index.htm

Maybe the way to deal with PD is to try and stop neuro-inflammation. Naltrexone and dextromethorphan are cheap, safe and in the case of DM easily available. I have been taking LDN now for 47 months plus 600mg of Q10. My overall combo of sinemet and mirapex has not increased over that time. But, maybe like Robert, I am still early onset and the other shoe has yet to drop.
Ashley
http://www.ncbi.nlm.nih.gov/pubmed/1...?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pubmed/1...?dopt=Abstract

This is a post from the Yahoo lowdosenaltrexone web site on naltrexone clinical studies. I guess what I take away from this is that these are more papers showing that naltrexone is a real oipioid type drug that does effect the immune system and that it does not seem to damage the liver. Also, keep in mind that for treatment of many diseases, MS, PD etc., naltrexone is used at low doses (3 - 10 mg) as shown by Zagon and Hong studies. Doses above 10mg may be countrproductive.

Ashley




Hello All,
As a follow up to Message Naltrexone and the Liver Warning Explained (Part 1) - Clinical Trial and to further clarify recent discussions about Naltrexone and the liver, I've included below an excerpt from information on the Hepatitis_Children_and_CAM_Alternatives Yahoo Group. The below are nine Clinical Studies which demonstrate the safety and very beneficial effects of Naltrexone to the liver for dosages below 300 mg a day in those with pre-existing liver disease (Hepatitis, Billary Cirrhosis, Cholestasis, Fibrosis, etc.). While the below are not specific to Low Dose Naltrexone (which is taken in much smaller dosages of approximately 1 to 4.5 mg a day), the below studies demonstrate the beneficial affect that opioid antagonists can have in liver disease. Please feel free to discuss the below clinical studies with your doctor.

Hope this helps!
~~ J

Naltrexone – How it Helps the Liver
Our body's own immune systems is influenced by opioids and opioid receptors:
"…….Up to the present time, the question of "What controls the immune system?" has not been present in the curricula of medical colleges and the issue has not formed a part of the received wisdom of practicing physicians. Nonetheless, a body of research over the past two decades has pointed repeatedly to one's own endorphin secretions (our internal opioids) as playing the central role in the beneficial orchestration of the immune system, and recognition of the facts is growing.
Witness these statements from a review article of medical progress in the November 13, 2003 issue of the prestigious New England Journal of Medicine: "Opioid-Induced Immune Modulation: .... Preclinical evidence indicates overwhelmingly that opioids alter the development, differentiation, and function of immune cells, and that both innate and adaptive systems are affected.1,2 Bone marrow progenitor cells, macrophages, natural killer cells, immature thymocytes and T cells, and B cells are all involved. The relatively recent identification of opioid-related receptors on immune cells makes it even more likely."
-- Quoted from (http://www.ldninfo.org/index.htm#Wha...ose_naltrexone)

Naltrexone is an opioid antagonist that has been shown to influence the immune system:
"Naltrexone, an opioid antagonist, has been used in clinical trials to treat alcoholism. . We conclude that naltrexone, …may have potential use in the treatment of immune deficiency in alcoholic and nonalcoholic patients…… we report in this study that chronic naltrexone administration in laboratory rats increases the cytolytic activity of NK cells …..Natural killer cells are lymphocytes that participate in the body's immune defense system by killing bacteria, viruses, and cancer cells. NK cells quickly respond to immune activation signals, and activated NK cells circulate through blood and lymph and accumulate at the sites of injuries, infections, and tumors (1, 2, 3)." - The Journal of Immunology, 2004, 173: 42-49. (http://www.jimmunol.org/cgi/content/full/173/1/42)
Opioid Antagonist Naltrexone Disrupts Feedback Interaction between µ and Opioid Receptors in Splenocytes to Prevent Alcohol Inhibition of NK Cell Function1 -- By Nadka I. Boyadjieva, Kirti Chaturvedi, Michael M. Poplawski and Dipak K. Sarkar2

Clinical Studies demonstrating Naltrexone's Beneficial Effects to the Liver:
The following are nine Clinical Studies which demonstrate the safety and very beneficial effects of Naltrexone to the liver for dosages below 300 mg a day. While the below are not specific to Low Dose Naltrexone (which is taken in much smaller dosages of approximately 1 to 4.5 mg a day), the below studies demonstrate the beneficial affect that opioid antagonists can have in liver disease in the following ways:
1.Reducing Liver Enzymes Levels, including Hepatitis (Studies 1 & 2)
2.Reducing Liver Damage in Hepatitis (Study 3)
3.Reducing Liver Injury in Cholestasis (Study 4)
4.Reducing Liver Enzymes in Cholestasis (Study 5)
5.Reducing Liver Fibrosis (Study 6)
6.Anti-inflammatory effects & improving hepatic dysfunction (Study 7)
7.Benefits in Cholestatic Pruritus (Studies 8 & 9)
All of the below Clinical Studies / Articles are quoted from the National Institutes of Health / National Library of Medicine/Pub Med Website:
(http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed)
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Study 1 – Benefit of reducing liver enzyme (ALT/AST) levels:
Study of hepatotoxicity of naltrexone in the treatment of alcoholism.
Alcohol. 2006 Feb;38(2):117-20. Links
Yen MH, Ko HC, Tang FI, Lu RB, Hong JS.
Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan.
Since a black box warning was issued by the Food and Drug Administration regarding the use of the opiate antagonist naltrexone (NTX), many clinicians have been concerned about current labeling of the potential hepatotoxicity risk of NTX in the treatment of opiate dependence and alcoholism. Despite many reports that demonstrated that the use of NTX did not cause elevation of liver enzymes, controversy concerning whether NTX is hepatotoxic continues. The current study monitored 74 alcoholic patients who received 25mg of NTX daily in the first week and then 50mg of NTX daily for the rest of the 12-week period. After the 12-week treatment, levels of the hepatic enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) did not show any elevation, except in one subject, and the results strongly support that NTX did not induce abnormalities in liver function tests or elevate the liver enzymes. Instead, a statistical significance of decreasing levels of ALT and AST in the liver was shown throughout the study. These findings provide further support that NTX is not hepatotoxic at the recommended daily dose and may be beneficial for patients with elevated liver enzymes.
PMID: 16839858 [PubMed - indexed for MEDLINE]
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Study 2 – Benefit of reducing liver enzyme levels in Hepatitis C patients:
Effect of methadone or naltrexone on the course of transaminases in parenteral drug users with hepatitis C virus infection

[Article in Spanish]
Lozano Polo JL, Gutiérrez Mora E, Martínez Pérez V, Santamaría Gutiérrez J, Vada Sánchez J, Vallejo Correas JA.
Hospital Santa Cruz de Liencres,Servico de Medicina Interna, Cantabria.
A prospective study was conducted on the evolution of serum transaminases in 116 patients infected with hepatitis C virus (HCV), parenteral drug abusers, included for 6 months in treatment programs with methadone, naltrexone or "drug free" regimen. Treatment with methadone or naltrexone did not result in a transaminase increase in these patients. In contrast, patients included in the drug-free program appear to have a higher increase in serum transaminase levels than those treated with methadone or naltrexone (146.1 +/- 122.29 vs 91.88 +/- 81.96 and 86.99 +/- 64.26 Ul/ml, respectively). Such an increase originated mainly from patients who anytime during follow-up had a liver necrosis outbreak in the acute hepatitis range, and is offset if, instead of a given transaminase value, we consider a simplified liver necrosis index (1.28 +/- 0.74 vs 0.95 +/- 0.72 and 1.01 +/- 0.65, respectively; p > 0.05). HIV infected patients have serum transaminase values similar to those in HIV-negative patients (80.61 +/- 58.81 vs 113.63 +/- 99.59, respectively; p > 0.05).
PMID: 9411543 [PubMed - indexed for MEDLINE]
Note: Basically, the above study showed that ALT/AST levels of those with Hepatitis C who used Naltrexone, had liver enzymes significantly lower (86.99 +/- 64.26) than those patients who did not use Naltrexone (i.e. were `drug free' – 146.1 +/- 122.29)
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Study 3 – Benefit by reducing liver damage of hepatitis:
Opioid receptor blockade reduces Fas-induced hepatitis in mice.

Hepatology. 2004 Nov;40(5):1136-43.
Jaume M, Jacquet S, Cavaillès P, Macé G, Stephan L, Blanpied C, Demur C, Brousset P, Dietrich G.
INSERM U563, Institut Claude de Préval, IFR 30, Hôpital Purpan, Université Paul Sabatier Toulouse III, Toulouse, France.
Fas (CD95)-induced hepatocyte apoptosis and cytotoxic activity of neutrophils infiltrating the injured liver are two major events leading to hepatitis. Because it has been reported that opioids, via a direct interaction, sensitize splenocytes to Fas-mediated apoptosis by upregulating Fas messenger RNA (mRNA) and modulated neutrophil activity, we assumed that opioids may participate in the pathophysiology of hepatitis. Using the hepatitis model induced by agonistic anti-Fas antibody in mice, we showed that opioid receptor blockade reduced liver damage and consequently increased the survival rate of animals when the antagonist naltrexone was injected simultaneously or prior to antibody administration. Treatment of mice with morphine enhanced mortality. Naloxone methiodide-a selective peripheral opioid antagonist-had a protective effect, but the absence of opioid receptors in the liver, together with lack of morphine effect in Fas-induced apoptosis of primary cultured hepatocytes, ruled out a direct effect of opioids on hepatocytes. In addition, the neutralization of opioid activity by naltrexone did not modify Fas mRNA expression in the liver as assessed with real-time quantitative polymerase chain reaction. Injured livers were infiltrated by neutrophils, but granulocyte-depleted mice were not protected against the enhancing apoptotic effect of morphine. In conclusion, opioid receptor blockade improves the resistance of mice to Fas-induced hepatitis via a peripheral mechanism that does not involve a down-modulation of Fas mRNA in hepatocytes nor a decrease in proinflammatory activity of neutrophils.
PMID: 15389866 [PubMed - indexed for MEDLINE]

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Study 4 – Benefit of reducing liver injury:
Opioid system blockade decreases collagenase activity and improves liver injury in a rat model of cholestasis.
J Gastroenterol Hepatol. 2007 Mar;22(3):406-13.
Kiani S, Ebrahimkhani MR, Shariftabrizi A, Doratotaj B, Payabvash S, Riazi K, Dehghani M, Honar H, Karoon A, Amanlou M, Tavangar SM, Dehpour AR.
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
BACKGROUND: Following bile duct ligation (BDL) endogenous opioids accumulate in plasma and play a role in the pathophysiology and manifestation of cholestasis. Evidence of centrally mediated induction of liver injury by exogenous opioid agonist administration, prompts the question of whether opioid receptor blockade by naltrexone can affect cholestasis-induced liver injury.
METHODS: Cholestasis was induced by BDL and cholestatic and sham-operated rats received either naltrexone or saline for 7 consecutive days. On the 7th day, liver samples were collected for determining matrix metalloproteinase-2 (MMP-2) activity, S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) content and blood samples were obtained for measuring plasma nitrite/nitrate and liver enzyme activities.
RESULTS: Naltrexone-treated BDL animals had a significant reduction in plasma enzyme activity and nitrite/nitrate level. Liver SAM : SAH ratio and SAM level improved by naltrexone treatment in cholestatic animals compared to saline-treated BDL ones. Naltrexone treatment in BDL rats led to a decrease in the level of liver MMP-2 activity, which had already increased during cholestasis.
CONCLUSION: Opioid receptor blockade improved the degree of liver injury in cholestasis, as assessed by plasma enzyme and liver MMP-2 activities. The beneficial effect of naltrexone may be due to its ability to increase liver SAM level and restore the SAM : SAH ratio.
PMID: 17295775 [PubMed - indexed for MEDLINE]
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Study 5– Reducing Liver Enzymes in Cholestatis
Do endogenous opioids contribute to the bradycardia of rats with obstructive cholestasis?
Fundam Clin Pharmacol. 2002 Aug;16(4):273-9.
Gaskari SA, Mani AR, Ejtemaei-Mehr S, Namiranian K, Homayoun H, Ahmadi H, Dehpour AR.
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Endogenous opioids have nitric oxide (NO)-dependent cardiovascular actions. In the light of biological evidence of accumulation of endogenous opioids in cholestasis and also existence of NO-dependent bradycardia in cholestatic subjects, this study was carried out to evaluate the role of endogenous opioids in the generation of bradycardia in a rat model of cholestasis. Male Sprague-Dawley rats were used to induce cholestasis by surgical ligation of the bile duct, with sham-operated animals serving as a control. The animals were divided into six groups which received naltrexone [20 mg/kg/day, subcutaneously (s.c.)], N(G)-L-nitro-arginine methyl ester (L-NAME, 3 mg/kg/day, s.c.), aminoguanidine (200 mg/kg/day, s.c.), L-arginine (200 mg/kg/day, s.c.), naltrexone + L-NAME (20 and 3 mg/kg/day, s.c) or saline. One week after the operation, a lead II electrocardiogram (ECG) was recorded and the spontaneously beating atria of the animals were then isolated and the chronotropic responses to epinephrine evaluated. The plasma L-nitro-tyrosine level and alanine amino transferase and alkaline phosphatase activities were also measured. The heart rate of cholestatic animals was significantly lower than that of control rats in vivo and this bradycardia was corrected with daily adminstration of naltrexone or L-NAME. The basal spontaneous beating rate of atria in cholestatic animals was not significantly different from that of sham-operated animals in vitro. Cholestasis induced a significant decrease in the chronotropic effect of epinephrine. This effect was corrected by daily injection of naltrexone or L-NAME, or concurrent administration of naltrexone + L-NAME, and was not corrected by aminoguanidine. L-arginine had an equivalent effect to L-NAME and increased the chronotropic effect of epinephrine in cholestatic rats but not in control animals. Bile duct ligation increased the plasma activity of liver enzymes as well as the level of L-nitro-tyrosine. L-arginine and naltrexone treatment significantly decreased the elevation of liver enzymes in bile duct-ligated rats. Pretreatment of cholestatic animals with naltrexone or L-NAME decreased the plasma L-nitro-tyrosine level. The results suggest that either prevention of NO overproduction or protection against liver damage is responsible for recovery of bradycardia after naltrexone administration.
PMID: 12570015 [PubMed - indexed for MEDLINE]
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Study 6– Benefit of reducing liver fibrosis:

Naltrexone, an opioid receptor antagonist, attenuates liver fibrosis in bile duct ligated rats.
Gut. 2006 Nov;55(11):1606-16. Epub 2006 Mar 16.
Ebrahimkhani MR, Kiani S, Oakley F, Kendall T, Shariftabrizi A, Tavangar SM, Moezi L, Payabvash S, Karoon A, Hoseininik H, Mann DA, Moore KP, Mani AR, Dehpour AR.
The UCL Institute of Hepatology, Department of Medicine, Royal Free and University College Medical School, University College London, Rowland Hill St, London NW3 2PF, UK.
AIM: The aim of this study was to investigate the hypothesis that the opioid system is involved in the development of hepatic fibrosis.
METHODS: The effect of naltrexone (an opioid receptor antagonist) on hepatic fibrosis in bile duct ligated (BDL) or sham rats was assessed by histology and hepatic hydroxyproline levels. Liver matrix metalloproteinase 2 (MMP-2) was measured by zymography, and alpha smooth muscle actin (alpha-SMA) and CD45 (leucocyte common antigen) by immunohistochemistry. The redox state of the liver was assessed by hepatic glutathione (GSH)/oxidised glutathione (GSSG) and S-nitrosothiol levels. Subtypes of opioid receptors in cultured hepatic stellate cells (HSCs) were characterised by reverse transcriptase-polymerase chain reaction, and the effects of selective delta opioid receptor agonists on cellular proliferation, tissue inhibitor of metalloproteinase 1 (TIMP-1), and procollagen I expression in HSCs determined.
RESULTS: Naltrexone markedly attenuated the development of hepatic fibrosis as well as MMP-2 activity (p<0.01), and decreased the number of activated HSCs in BDL rats (p<0.05). The development of biliary cirrhosis altered the redox state with a decreased hepatic GSH/GSSG ratio and increased concentrations of hepatic S-nitrosothiols, which were partially or completely normalised by treatment with naltrexone, respectively. Activated rat HSCs exhibited expression of delta1 receptors, with increased procollagen I expression, and increased TIMP-1 expression in response to delta(1) and delta(2) agonists, respectively.
CONCLUSIONS: This is the first study to demonstrate that administration of an opioid antagonist prevents the development of hepatic fibrosis in cirrhosis. Opioids can influence liver fibrogenesis directly via the effect on HSCs and regulation of the redox sensitive mechanisms in the liver.
PMID: 16543289 [PubMed - indexed for MEDLINE]
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Study 7– Benefit of anti-inflammatory effects & improving hepatic dysfunction:
Effects of naltrexone on lipopolysaccharide-induced sepsis in rats.
J Biomed Sci. 2005;12(2):431-40. Links
Lin SL, Lee YM, Chang HY, Cheng YW, Yen MH.
Department of Anesthesiology, Tri-Service General Hospital, Taipei, Taiwan.
Naltrexone, an opioid antagonist, has been reported to possess an anti-inflammatory effect via blockade of opioid receptor. The aim of this study is to evaluate the protective effect of naltrexone on LPS-induced septic shock in rats. Sepsis was induced by administration of LPS (10 mg/kg, i.v.) in anesthetized rats. Results demonstrated that pretreatment with naltrexone (10 mg/kg, i.v.) significantly ameliorated hypotension and bradycardia of rats 6 h after LPS administration. In isolated blood vessel, study showed that pretreatment with naltrexone significantly improved norepinephrine-induced vasoconstriction and ACh-induced vasorelaxation in aorta of endotoxemic animals. Naltrexone significantly reduced the elevation of serum glutamate-oxalacetate transaminase and glutamate-pyruvate transaminase (as index of hepatic function) induced by LPS. The infiltration of polymorphonuclear neutrophils into liver 48 h after LPS treatment in mice was also reduced by naltrexone. On the other hand, naltrexone significantly decreased the levels of plasma TNF-alpha and inhibited overproduction of superoxide anions in aortic rings. However, naltrexone did not suppress the overproduction of NO (measured by its metabolites nitrite/nitrate in plasma) and iNOS expression in lungs induced by LPS. In in vitro study, naltrexone did not attenuate non-enzymatic iron-induced lipid peroxidation in rat brain homogenates. In conclusion, pretreatment with naltrexone significantly improved circulatory failure and hepatic dysfunction in sepsis. These effects were associated with reduction of TNF-alpha levels and superoxide anion formation, which may be attributed to antagonism of opioid receptors.
PMID: 15917999 [PubMed - indexed for MEDLINE]
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Study 8 – Benefits in Cholestatic Pruritus:

Oral naltrexone treatment for cholestatic pruritus: a double-blind, placebo-controlled study.
Gastroenterology. 1997 Oct;113(4):1264-9.
Wolfhagen FH, Sternieri E, Hop WC, Vitale G, Bertolotti M, Van Buuren HR.

Department of Hepatogastroenterology, University Hospital Rotterdam-Dijkzigt, The Netherlands.

BACKGROUND & AIMS: The efficacy of currently available therapeutic agents for cholestatic pruritus is often disappointing. The aim of this study was to assess the antipruritic effect of naltrexone, an oral opiate receptor antagonist.
METHODS: Sixteen patients with pruritus of chronic cholestasis were randomized to receive naltrexone (4-week course of 50 mg naltrexone daily) or placebo. Pruritus, quality of sleep, fatigue (using visual analogue scales), side effects, and liver function were assessed every 2 weeks. Serum naltrexone and 6 beta-naltrexol concentrations in all patients and 5 healthy controls were measured during the first day of naltrexone treatment.
RESULTS: Mean changes with respect to baseline were significantly different, in favor of the naltrexone group, for daytime itching (-54% vs. 8%; P < 0.001) and nighttime itching (-44% vs. 7%, P = 0.003). In 4 naltrexone-treated patients, side effects (transient in 3 cases) consistent with an opiate withdrawal syndrome were noted. No deterioration of the underlying disease was observed. Naltrexone and 6 beta-naltrexol levels did not differ between patients and controls, and there was no significant association with treatment response.
CONCLUSIONS: For patients with cholestatic liver disease and itching, refractory to regular antipruritic therapy, oral naltrexone may be an effective and well-tolerated alternative.PMID: 9322521 [PubMed - indexed for MEDLINE]
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Study 9 – Benefits in Pruritus for liver disease:

Antipruritic therapy with the oral opioid receptor antagonist naltrexone. Open, non-placebo controlled administration in 133 patients
Hautarzt. 2004 Dec;55(12):1130-6.
[Article in German]

Brune A, Metze D, Luger TA, Ständer S.

Klinik und Poliklinik für Hautkrankheiten, Universitätsklinikum Münster.

BACKGROUND AND OBJECTIVES: The perception of pruritus is modified by endogenous and exogenous opioids via central opiate receptors and can be suppressed with opioid receptor antagonists. The aim of this investigation was to describe the efficacy and safety of naltrexone, an orally active opiate antagonist, in the treatment of severe, otherwise intractable pruritus of varying origins.
PATIENTS: A total of 133 patients with pruritus caused by inflammatory skin diseases (asteatotic dermatitis, atopic dermatitis, prurigo, and psoriasis vulgaris), liver- and renal diseases, cutaneous lymphoma, as well as with pruritus of unknown origin were treated with naltrexone (Nemexin) 50 to 150 mg daily.
RESULTS: A therapeutic response was achieved in 86 of the 133 (64.6%) patients. Naltrexone was most effective in prurigo nodularis, cutaneous lymphoma and pruritus of unknown origin. Tachyphylaxis occurred in 13% of the patients, but appeared late, and could be counterbalanced by raising the dosage. Adverse drug effects were restricted to the first two weeks of treatment and included mainly neurological (dizziness, headache, fatigue) and gastrointestinal (nausea, vomiting, diarrhea) symptoms.
CONCLUSIONS: The oral opiate antagonists may well be an effective, well-tolerated therapy for intractable pruritus in many diseases.


PMID: 15517116 [PubMed - indexed for MEDLINE]
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All of the above Clinical Trials were quoted from the National Institutes of Health/National Library of Medicine.
Note regarding National Institutes of Health / National Library of Medicine Copyright / Public Domain information - quoted from (http://www.nlm.nih.gov/copyright.html).
NLM Copyright Information
Government information at NLM Web sites is in the public domain. Public domain information may be freely distributed and copied, but it is requested that in any subsequent use the National Library of Medicine (NLM) be given appropriate acknowledgement. When using NLM Web sites, you may encounter documents, illustrations, photographs, or other information resources contributed or licensed by private individuals, companies, or organizations that may be protected by U.S. and foreign copyright laws. Transmission or reproduction of protected items beyond that allowed by fair use (PDF) as defined in the copyright laws requires the written permission of the copyright owners. Specific NLM Web sites containing protected information provide additional notification of conditions associated with its use.

HEARD IT CAN BE DANGEROUS

Naltrexone may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away:

upset stomach
anxiety
nervousness
muscle or joint pain

If you experience any of the following symptoms or those listed in the IMPORTANT WARNING section, call your doctor immediately:

confusion
drowsiness
hallucinations
vomiting
diarrhea
bone and joint pain
skin crawling
stomach pain
white bowel movements
skin rash
blurred vision

Have you looked at a similar list for Sinemet? Now, that's scary.