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Re: subotex=suboxone

Post by Visions » Wed Jul 21, 2010 3:02 pm

Pa da, ali nikako nemoj to da radis.Reci svom Dr-u i dobices nesto sto smes da koristis uz taj lek.Postoje ljudi koj su dugogodisnji alkoholicari ili su preko 10 godina na benzodiazepinima pa su postali imuni,tolerantni i zavisni.Oni to moraju tako bez obzira na rizik.Zato neslusaj njihova hvalisanja vec idi i trazi nesto za spavanje ili sta ti vec treba.

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Re: subotex=suboxone

Post by Migoda » Sat Sep 18, 2010 3:49 am

Koliko smo para davali na drogu a sad nam je suboxon skup. Dajte te priče su su samo da se čovek istrese i ako je to bio cilj dobro. Medjutim, ako me suboxon skine sa dopa bez krize platiću i više ako treba. :roll:

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Re: subotex=suboxone

Post by drevil » Fri Sep 24, 2010 8:53 am

Evo malo naučnih činjenica, bar tako farmaceuti kažu.

Drug Nomenclature
Date of monograph revision: 13-Aug-1998; 07-Mar-2000; 06-Nov-2001; 08-Aug-2003; 26-May-2004; 31-May-2006; (last modified: 28-Jun-2006)
Synonyms: Buprenorfiini; Buprenorfin; Buprenorfina; Buprenorfinas; Buprenorphinum; RX-6029-M
BAN: Buprenorphine [BAN]
INN: Buprenorphine [rINN (en)]
INN: Buprenorfina [rINN (es)]
INN: Buprénorphine [rINN (fr)]
INN: Buprenorphinum [rINN (la)]
INN: Бупренорфин [rINN (ru)]
Chemical name: (6R,7R,14S)-17-Cyclopropylmethyl-7,8-dihydro-7-[(1S)-1-hydroxy-1,2,2-trimethylpropyl]-6-O-methyl-6,14-ethano-17-normorphine; (2S)-2-[(-)-(5R,6R,7R,14S)-9a-Cyclopropylmethyl-4,5-epoxy-3-hydroxy-6-methoxy-6,14-ethanomorphinan-7-yl]-3,3-dimethylbutan-2-ol
Molecular formula: C29H41NO4 =467.6
CAS: 52485-79-7
ATC code: N02AE01; N07BC01
Read code: y02Aq

Chemical Structure of Buprenorphine

NOTE: The following terms have been used as 'street names' (see ) or slang names for various forms of buprenorphine:

Use in Sport. Buprenorphine may be restricted in certain sports (see ) and competitors should check with the appropriate sports authorities.

In Eur. (see ).

Ph. Eur. 5.5 (Buprenorphine). A white or almost white crystalline powder. Very slightly soluble in water; freely soluble in acetone; slightly soluble in cyclohexane; soluble in methyl alcohol. It dissolves in dilute solutions of acids. Protect from light.

Buprenorphine Hydrochloride
Drug Nomenclature
Date of monograph revision: 24-Oct-1997; 13-Aug-1998; 07-Mar-2000; 06-Nov-2001; 08-Aug-2003; 26-May-2004; 31-May-2006; (last modified: 28-Jun-2006)
Synonyms: Buprenorfiinihydrokloridi; Buprenorfin-hidroklorid; Buprenorfin-hydrochlorid; Buprenorfina, hidrocloruro de; Buprenorfinhydroklorid; Buprenorfino hidrochloridas; Buprenorphini Hydrochloridum; CL-112302; NIH-8805; UM-952
BAN: Buprenorphine Hydrochloride [BANM]
USAN: Buprenorphine Hydrochloride
INN: Buprenorphine Hydrochloride [rINNM (en)]
INN: Hidrocloruro de buprenorfina [rINNM (es)]
INN: Buprénorphine, Chlorhydrate de [rINNM (fr)]
INN: Buprenorphini Hydrochloridum [rINNM (la)]
INN: Бупренорфина Гидрохлорид [rINNM (ru)]
Molecular formula: C29H41NO4,HCl =504.1
CAS: 53152-21-9
Use in Sport. Buprenorphine may be restricted in certain sports (see ) and competitors should check with the appropriate sports authorities.

In Chin., Eur. (see ), and US.

Ph. Eur. 5.5 (Buprenorphine Hydrochloride). A white or almost white crystalline powder. Sparingly soluble in water; soluble in alcohol; practically insoluble in cyclohexane; freely soluble in methyl alcohol. Protect from light.

USP 29 (Buprenorphine Hydrochloride). pH of a 1% solution in water is between 4.0 and 6.0. Store in airtight containers. Protect from light.

Dependence and Withdrawal
As for Opioid Analgesics, .

Buprenorphine may have a lower potential for producing dependence than pure agonists such as morphine. However, it has been subject to abuse. Abrupt withdrawal of buprenorphine is said to produce only a mild abstinence syndrome.

Adverse Effects and Treatment
As for Opioid Analgesics in general, .

Local reactions such as rash, erythema, and itching have been reported with the transdermal patches. In isolated cases delayed local allergic reactions with marked signs of inflammation have occurred; the patches should be withdrawn in such cases.

Treatment of adverse effects is similar to that for other opioid analgesics (). The effects of buprenorphine are only partially reversed by naloxone (see under Effects on the Respiratory System, ) but use of the latter is still recommended.

Incidence of adverse effects.
Adverse effects reported1 after buprenorphine injection in 8187 patients were nausea (8.8%), vomiting (7.4%), drowsiness (4.3%), sleeping (1.9%), dizziness (1.2%), sweating (0.98%), headache (0.55%), confusion (0.53%), lightheadedness (0.38%), blurred vision (0.28%), euphoria (0.27%), dry mouth (0.11%), depression (0.09%), and hallucinations (0.09%). Some studies have reported nausea, vomiting, and dizziness to be more troublesome with buprenorphine than with morphine.2,3

In a trial of sublingual buprenorphine 50 of 141 cancer patients withdrew because of side-effects, especially dizziness, nausea, vomiting, and drowsiness; constipation was not reported.4 A woman developed a painless ulcer on the upper surface of her tongue after she had put sublingual buprenorphine tablets on rather than under her tongue.5

Shock occurred6 in 2 patients 2 hours after receiving epidural buprenorphine 300 micrograms; treatment with naloxone was unsuccessful but symptoms disappeared spontaneously after 2 to 3 hours.

1. Harcus AW, et al Methodology of monitored release of a new preparation: buprenorphine. BMJ 1979; 2: 163–5. PubMed
2. Sear JW, et al. Buprenorphine for postoperative analgesia. Br J Anaesth 1979; 51: 71. PubMed
3. Kjaer M, et al. A comparative study of intramuscular buprenorphine and morphine in the treatment of chronic pain of malignant origin. Br J Clin Pharmacol 1982; 13: 487–92. PubMed
4. Robbie DS. A trial of sublingual buprenorphine in cancer pain. Br J Clin Pharmacol 1979; 7 (suppl 3): 315S–17S. PubMed
5. Lockhart SP, Baron JH. Tongue ulceration after lingual buprenorphine. BMJ 1984; 288: 1346.
6. Christensen FR, Andersen LW. Adverse reaction to extradural buprenorphine. Br J Anaesth 1982; 54: 476. PubMed
Effects on the heart.
For a report of myocardial infarction associated with abuse of buprenorphine, see Abuse under Precautions, .

Effects on mental function.
Psychotomimetic effects have been relatively uncommon with buprenorphine. Hallucinations were reported1 in only 7 of 8147 patients (0.09%) given buprenorphine by injection. There have been reports of hallucinations after sublingual2 or epidural3 administration.

1. Harcus AW, et al. Methodology of monitored release of a new preparation: buprenorphine. BMJ 1979; 2: 163–5. PubMed
2. Paraskevaides EC. Near fatal auditory hallucinations after buprenorphine. BMJ 1988; 296: 214. PubMed
3. MacEvilly M, O'Carroll C. Hallucinations after epidural buprenorphine. BMJ 1989; 298: 928–9. PubMed
Effects on the respiratory system.
There have been varying reports on the occurrence of respiratory depression with buprenorphine. It may be subject to a 'ceiling effect' in which respiratory depression does not increase further above doses of about 3 micrograms/kg.1 However, high doses of 30 or 40 micrograms/kg given as sole intravenous analgesic in balanced anaesthesia have been associated with severe respiratory depression.2

Respiratory depression may be delayed in onset and more prolonged than with morphine and is only partially reversed by naloxone, possibly because buprenorphine is very firmly bound to opioid receptors. A study of sublingual buprenorphine for postoperative pain relief was abandoned when 3 of the first 16 patients showed signs of late-onset respiratory depression after the second dose of buprenorphine; the respiratory depression did not respond to naloxone.3 Successful reversal has been demonstrated in healthy subjects with buprenorphine-induced respiratory depression given large doses of naloxone 5 or 10 mg, but not with 1 mg; reversal was gradual in onset and decreased the duration of the normally prolonged respiratory depression.4 The respiratory depressant and analgesic effects of buprenorphine were decreased by the concomitant use of naloxone.5

1. Dahan A, et al. Comparison of the respiratory effects of intravenous buprenorphine and fentanyl in humans and rats. Br J Anaesth 2005; 94: 825–34. PubMed
2. Schmidt JF, et al. Postoperative pain relief with naloxone: severe respiratory depression and pain after high dose buprenorphine. Anaesthesia 1985; 40: 583–6. PubMed
3. Thörn S-E, et al. Prolonged respiratory depression caused by sublingual buprenorphine. Lancet 1988; i: 179–80. PubMed
4. Gal TJ. Naloxone reversal of buprenorphine-induced respiratory depression. Clin Pharmacol Ther 1989; 45: 66–71. PubMed
5. Lehmann KA, et al. Influence of naloxone on the postoperative analgesic and respiratory effects of buprenorphine. Eur J Clin Pharmacol 1988; 34: 343–52. PubMed
As for Opioid Analgesics in general, .

Buprenorphine has opioid antagonist actions and may precipitate withdrawal symptoms if given to patients physically dependent on opioids.

Respiratory depression, if it occurs, is relatively slow in onset and of prolonged duration; it may be only partially reversed by naloxone.

Absorption of buprenorphine from transdermal patches may be increased as the temperature rises and patients should therefore avoid exposing the patch to external heat; similarly, patients with fever may require monitoring because of increased absorption. It may take 30 hours for plasma concentrations of buprenorphine to decrease by 50% after removal of a patch; patients who have experienced adverse effects should be monitored during this period.

A 22-year-old man experienced chest pains on each of two occasions after he had inhaled crushed buprenorphine tablets.1 An ECG taken after the second episode suggested that the patient had suffered a myocardial infarction. Intravenous injection of crushed sublingual tablets was associated with rhabdomyolysis and sciatic neuropathy in 2 patients.2 The use of adulterants in illicit preparations may also cause adverse effects: 4 patients on substitution treatment developed candida endophthalmitis after intravenously injecting sublingual buprenorphine diluted with lemon juice.3

1. Cracowski J-L, et al. Myocardial infarction associated with buprenorphine. Ann Intern Med 1999; 130: 537. PubMed
2. Seet RCS, Lim ECH. Intravenous use of buprenorphine tablets associated with rhabdomyolysis and compressive sciatic neuropathy. Ann Emerg Med 2006; 47: 396–7. PubMed
3. Cassoux N, et al. Presumed ocular candidiasis in drug misusers after intravenous use of oral high dose buprenorphine (Subutex). Br J Ophthalmol 2002; 86: 940–1. PubMed
Breast feeding.
The BNF considers that the amount of buprenorphine distributed into breast milk is probably too small to be harmful to a breast-fed infant. However, licensed product information states that buprenorphine should not be used for substitution treatment in opioid-dependent mothers who are breast feeding.

From a study1 of a breast-feeding mother who was receiving buprenorphine 4 mg daily, it was estimated that at the age of 4 weeks the total amount ingested by the infant during a 24-hour period was 3.28 micrograms for buprenorphine and 0.33 micrograms for norbuprenorphine.

1. Marquet P, et al. Buprenorphine withdrawal syndrome in a newborn. Clin Pharmacol Ther 1997; 62: 569–71. PubMed
An infant born to a mother who was being treated with buprenorphine 4 mg daily for diamorphine addiction suffered a minor withdrawal syndrome 2 days after birth.1 The infant rapidly recovered without any treatment. No further signs of withdrawal occurred when breast feeding was abruptly stopped at the age of 8 weeks. In another report2 of 15 opioid-dependent mothers who had received buprenorphine maintenance during their pregnancies, withdrawal symptoms were either absent or mild in 12 of the neonates. The remaining 3 neonates required treatment with morphine. There appeared to be no correlation between the buprenorphine dose and the degree of withdrawal symptoms.

1. Marquet P, et al. Buprenorphine withdrawal syndrome in a newborn. Clin Pharmacol Ther 1997; 62: 569–71. PubMed
2. Fischer G, et al. Treatment of opioid-dependent pregnant women with buprenorphine. Addiction 2000; 95: 239–44. PubMed
For interactions associated with opioid analgesics, see . Buprenorphine is metabolised by the cytochrome P450 isoenzyme CYP3A4; consequently, use with other drugs that induce or inhibit this isoenzyme may result in changes in plasma concentrations of buprenorphine and, possibly adverse effects. The dose of buprenorphine should be halved when starting treatment with the potent CYP3A4 inhibitor, ketoconazole; a similar reduction should be considered with other CYP3A4 inhibitors.

There is a risk that, with opioid agonist-antagonists such as buprenorphine, their antagonistic effects might impair more effective analgesic therapy. This appeared to happen in 2 cancer patients both of whom were given sublingual buprenorphine that was later substituted by morphine.1 Conventional doses of morphine were inadequate and in one patient raising the dose of morphine proved fatal.

1. Overweg-van Kints J, Stricker BHC. Falende pijnbestrijding tijdens sublinguaal gebruik van buprenorfine. Ned Tijdschr Geneeskd 1987; 131: 1973–4. PubMed
After intramuscular injection, buprenorphine rapidly reaches peak plasma concentrations. Absorption also takes place through the buccal mucosa after sublingual doses and peak plasma concentrations are achieved after 90 minutes. Transdermal application results in absorption through the skin; the minimum effective concentration is reached in 12 to 24 hours and peak plasma concentrations are achieved after about 60 hours. Buprenorphine is about 96% bound to plasma proteins. Plasma elimination half-lives have ranged from 1.2 to 7.2 hours; there is a lack of correlation between plasma concentrations and analgesic activity. Metabolism takes place in the liver by oxidation via the cytochrome P450 isoenzyme CYP3A4 to N-dealkylbuprenorphine (norbuprenorphine), and by conjugation to glucuronide metabolites. Buprenorphine is subject to considerable first-pass metabolism after oral doses. However, when given by the usual routes buprenorphine is excreted predominantly unchanged in the faeces; there is some evidence for enterohepatic recirculation. The terminal elimination half-life after sublingual doses is 20 to 25 hours; elimination following transdermal application is slower, with a half-life of about 30 hours. Metabolites are excreted in the urine, but very little unchanged drug is excreted in this way. Small amounts of buprenorphine are distributed into breast milk.


1. Elkader A, Sproule B. Buprenorphine: clinical pharmacokinetics in the treatment of opioid dependence. Clin Pharmacokinet 2005; 44: 661–80. PubMed
Buccal route.
Absorption of sublingual buprenorphine is relatively slow. In a 10-hour study1 plasma concentrations following 400 or 800 micrograms sublingually peaked at about 200 minutes (range 90 to 360 minutes) and buprenorphine was still detected in plasma at the end of the study. Systemic availability was about 55% (range 16 to 94%) and absorption was more or less complete 5 hours after a dose. However, the authors of a subsequent study2 considered that this was an overestimation, possibly due to methodological flaws. The later study results indicated that the bioavailability of sublingual buprenorphine is about 30% and that sublingual holding times between 3 and 5 minutes are bioequivalent. Another study found that the bioavailability of sublingual buprenorphine was 50% less from a tablet than from a liquid formulation.3

1. Bullingham RES, et al Sublingual buprenorphine used postoperatively: ten hour plasma drug concentration analysis. Br J Clin Pharmacol 1982; 13: 665–73. PubMed
2. Mendelson J, et al. Bioavailability of sublingual buprenorphine. J Clin Pharmacol 1997; 37: 31–7. PubMed
3. Nath RP, et al. Buprenorphine pharmacokinetics: relative bioavailability of sublingual tablet and liquid formulations. J Clin Pharmacol 1999; 39: 619–23. PubMed
The terminal elimination half-life of buprenorphine was only about 1 hour in small children aged 4 to 7 years given 3 micrograms/kg intravenously as premedication, but could not be estimated reliably because of the rapid decline in plasma-buprenorphine concentrations.1 Clearance values did however appear higher than in adults; steady-state volume of distribution was similar. Premature neonates (gestational age 27 to 32 weeks) given a similar dose followed by an infusion of 0.72 micrograms/kg per hour had a considerably lower clearance rate and had a mean elimination half-life of 20 hours.2 Although this dosing regimen appeared to be safe, sedation was judged to be inadequate in 4 of the 12 neonates studied. It was suggested that as buprenorphine given by infusion might not produce consistent sedation and analgesia in premature neonates, it could not be recommended for use in neonatal care.

1. Olkkola KT, et al. Pharmacokinetics of intravenous buprenorphine in children. Br J Clin Pharmacol 1989; 28: 202–4. PubMed
2. Barrett DA, et al. The pharmacokinetics and physiological effect of buprenorphine infusion in premature neonates. Br J Clin Pharmacol 1993; 36: 215–19. PubMed
Renal impairment.
Buprenorphine clearance appears to occur mainly by hepatic extraction and metabolism and would not be expected to be related to renal function, whereas metabolites are excreted in urine. In a study, buprenorphine kinetics were similar in anaesthetised healthy patients to those in patients with renal impairment, with a mean elimination half-life of 398 and 239 minutes, respectively.1 Plasma concentrations of the metabolites norbuprenorphine and buprenorphine-3-glucuronide were increased about 4 times and 15 times respectively in patients with renal impairment,1 but significant pharmacological activity was unlikely since norbuprenorphine has little analgesic activity compared with the parent compound and buprenorphine-3-glucuronide has none.

1. Hand CW, et al. Buprenorphine disposition in patients with renal impairment: single and continuous dosing, with special reference to metabolites. Br J Anaesth 1990; 64: 276–82. PubMed
Uses and Administration
Buprenorphine is an opioid analgesic () classified as an opioid agonist and antagonist. It is used for the relief of moderate to severe pain and as an adjunct to anaesthesia. Buprenorphine is also used in the treatment of opioid dependence.

Buprenorphine has a relatively slow onset but prolonged duration of action. On intramuscular injection analgesia is apparent within 15 minutes and lasts up to 6 hours. A slower, more prolonged response is achieved after sublingual doses. The analgesic effects of buprenorphine after transdermal application may not be seen for at least 12 to 24 hours or up to 72 hours in the case of the once-weekly patch.

Buprenorphine is usually given by intramuscular or intravenous injection or sublingually as the hydrochloride or as transdermal patches as the base. For all routes doses are expressed in terms of the base. Buprenorphine hydrochloride 107.8 micrograms is equivalent to about 100 micrograms of buprenorphine.

Buprenorphine is given by all the above routes for opioid analgesia in moderate to severe pain.

The dose by intramuscular or slow intravenous injection is 300 to 600 micrograms repeated every 6 to 8 hours as required. Children over 6 months may be given 3 to 6 micrograms/kg by injection every 6 to 8 hours; up to 9 micrograms/kg may be given if required in refractory cases

By the sublingual route, doses of 200 to 400 micrograms are given every 6 to 8 hours. Suggested sublingual doses for children over 6 years, also given every 6 to 8 hours, are: 16 to 25 kg, 100 micrograms; 25 to 37.5 kg, 100 to 200 micrograms; and 37.5 to 50 kg, 200 to 300 micrograms

For opioid treatment of chronic pain in adults transdermal patches delivering varying amounts of buprenorphine are available. Doses should be individually titrated for each patient according to previous opioid usage. During transfer to treatment with buprenorphine patches previous opioid analgesic therapy should be phased out gradually in order to allow for the gradual increase in plasma-buprenorphine concentrations. Depending on dose required up to 2 patches may be applied, however, this should be done at the same time to avoid confusion. Buprenorphine patches are not appropriate for acute pain In the UK, transdermal buprenorphine patches are available as follows:

Transtec (Napp, UK) delivering buprenorphine in a range of 35 to 70 micrograms/hour. Initial dosages should not exceed 35 micrograms/hour in opioid-naive patients. For patients who have been receiving a strong opioid analgesic the initial dose should be based on the previous 24-hour opioid requirement. Use of a patch providing 35 micrograms/hour of buprenorphine is roughly equivalent to 30 to 60 mg of morphine sulfate daily by mouth. Patches should be replaced every 96 hours at the latest with the new patch being applied to a different site; use of the same area of the skin should be avoided for at least the next 2 applications.

BuTrans (Napp, UK) delivering buprenorphine in a range of 5 to 20 micrograms/hour. Initial dosages should not exceed 5 micrograms/hour in all patients. Patches should be replaced every 7 days with the new patch being applied to a different site; use of the same area of the skin should be avoided for the next 3 to 4 weeks.

When used in balanced anaesthesia 300 micrograms may be given intramuscularly or 400 micrograms sublingually for premedication; 300 to 450 micrograms may be given intravenously as a perioperative analgesic supplement.

In the treatment of opioid dependence in adults and adolescents over 16 years, the initial dose is 0.8 to 4 mg sublingually once daily. The dose may be increased as necessary but maintenance doses should not exceed 32 mg daily. Once the patient has been stabilised, the dosage should be reduced gradually to a lower maintenance dose; treatment may eventually be discontinued if appropriate. For addicts who have not undergone opioid withdrawal before starting buprenorphine, the first dose of buprenorphine should not be given until the first signs of craving appear or until at least 4 hours after the last opioid use. In those already receiving methadone replacement, the dose of methadone should be reduced to a maximum of 30 mg daily before starting buprenorphine therapy. As a deterrent to abuse, a combined sublingual preparation of buprenorphine hydrochloride and naloxone hydrochloride is available in some countries for the treatment of opioid dependence.

Buprenorphine is generally described as a mixed agonist-antagonist acting mainly as a partial agonist at μ opioid receptors, with some antagonist activity at κ receptors. It has also been shown to bind at μ, δ, and κ opioid binding sites and to have high affinity for the μ and δ receptors and lesser affinity for the κ receptor.1 Buprenorphine, like fentanyl, has high lipid solubility, but has a lower intrinsic activity than fentanyl. Differences between buprenorphine and pure μ opioid agonists such as fentanyl, including relatively slow onset of action, prolonged duration of action, resistance to antagonism by naloxone, and lack of correlation between plasma concentrations and analgesic effects, have been explained by differences in the way buprenorphine binds to opioid receptors. In a study in vitro buprenorphine had slow rates of association and dissociation from the opioid receptor when compared with fentanyl.2

1. Bovill JG. Which potent opioid? Important criteria for selection. Drugs 1987; 33: 520–30. PubMed
2. Boas RA, Villiger JW. Clinical actions of fentanyl and buprenorphine: the significance of receptor binding. Br J Anaesth 1985; 57: 192–6. PubMed
In addition to its standard uses in anaesthesia (see ) buprenorphine was shown in a study1 to antagonise the respiratory rate depression following fentanyl as effectively as naloxone.

1. Boysen K, et al. Buprenorphine antagonism of ventilatory depression following fentanyl anaesthesia. Acta Anaesthesiol Scand 1988; 32: 490–2. PubMed
Opioid dependence.
Buprenorphine is used in the treatment of opioid dependence (). Its agonist-antagonist properties may mean that it has a lower potential for dependence and a lower risk of respiratory depression in overdose than pure agonists such as methadone. However, although it has potential in acute management of withdrawal, and is effective for maintenance, its place in clinical practice as an alternative to methadone remains to be proven. Abuse of the preparation, as with other substitution therapies, may be a problem. (A combined sublingual preparation of buprenorphine hydrochloride and naloxone hydrochloride is available in some countries as a deterrent to abuse.) In patients dependent on high doses of opioids buprenorphine may precipitate withdrawal due to its partial antagonist properties; the daily opioid dose should be reduced gradually in such patients before beginning buprenorphine.


1. Fudala PJ, et al. Use of buprenorphine in the treatment of opioid addiction: II physiologic and behavioural effects of daily and alternate-day administration and abrupt withdrawal. Clin Pharmacol Ther 1990; 47: 525–34. PubMed
2. Ling W, et al. A controlled trial comparing buprenorphine and methadone maintenance in opioid dependence. Arch Gen Psychiatry 1996; 53: 401–407. PubMed
3. O'Connor PG, et al. A randomized trial of buprenorphine maintenance for heroin dependence in a primary care clinic for substance users versus a methadone clinic. Am J Med 1998; 105: 100–105. PubMed
4. Kakko J, et al. year retention and social function after buprenorphine-assisted relapse prevention treatment for heroin dependence in Sweden: a randomised, placebo-controlled trial. Lancet 2003; 361: 662–8. PubMed
5. Fudala PJ, et al. Office-based treatment of opiate addiction with a sublingual-tablet formulation of buprenorphine and naloxone. N Engl J Med 2003; 349: 949–58. PubMed
6. Mattick RP, et al. Buprenorphine maintenance versus placebo or methadone maintenance for opioid dependence. Available in The Cochrane Database of Systematic Reviews; Issue 2. Chichester: John Wiley; 2003 (accessed 09/05/05). PubMed
7. Gowing L, et al. Buprenorphine for the management of opioid withdrawal. Available in The Cochrane Database of Systematic Reviews; Issue 4. Chichester: John Wiley; 2004 (accessed 24/10/05). PubMed
Acute pain.
The BNF considers that buprenorphine may antagonise the analgesic effect of other opioids and is generally not to be recommended for the management of postoperative pain. Nonetheless, it can be given intramuscularly, intravenously, or sublingually for this purpose, although the intravenous route may be preferred for acute pain relief. The epidural route has also been used.1 Patient-controlled analgesia with intravenous2 and intramuscular3 buprenorphine has been effective although its long half-life may limit such use.

Buprenorphine had no adverse cardiovascular effects when given intravenously after open-heart surgery,4 suggesting that it was a suitable analgesic for patients with unstable circulation. Epidural analgesia with buprenorphine has also been used after cardiac surgery.5 Buprenorphine was also considered suitable for the relief of pain in myocardial infarction.6

1. Miwa Y, et al. Epidural administered buprenorphine in the perioperative period. Can J Anaesth 1996; 43: 907–13. PubMed
2. Dingus DJ, et al. Buprenorphine versus morphine for patient-controlled analgesia after cholescystectomy. Surg Gynecol Obstet 1993; 177: 1–6. PubMed
3. Harmer M, et al. Intramuscular on demand analgesia: double blind controlled trial of pethidine, buprenorphine, morphine, and meptazinol. BMJ 1983; 286: 680–2. PubMed
4. Rosenfeldt FL, et al. Haemodynamic effects of buprenorphine after heart surgery. BMJ 1978; 2: 1602–3. PubMed
5. Mehta Y, et al. Lumbar versus thoracic epidural buprenorphine for postoperative analgesia following coronary artery bypass graft surgery. Acta Anaesthesiol Scand 1999; 43: 388–93. PubMed
6. Hayes MJ, et al. Randomised trial comparing buprenorphine and diamorphine for chest pain in suspected myocardial infarction. BMJ 1979; 2: 300–2. PubMed
Chronic pain.
Transdermal buprenorphine is used for chronic intractable cancer pain.1,2 It has also been used successfully in chronic non-cancer pain;1-3 however, the manufacturers state that this route is not suitable for the treatment of acute pain.

Naloxone Hydrochloride
Drug Nomenclature
Date of monograph revision: 01-Aug-1996; 22-May-1998; 12-Jul-1999; 23-Nov-2001; 26-Jun-2004; 16-Nov-2005; 12-Jul-2006
Synonyms: N-Allylnoroxymorphone Hydrochloride; Cloridrato de Naloxona; EN-15304; Naloksonihydrokloridi; Naloksono hidrochloridas; Naloxon-hidroklorid; Naloxon-hydrochlorid; Naloxona, hidrocloruro de; Naloxonhydroklorid; Naloxoni Hydrochloridum
BAN: Naloxone Hydrochloride [BANM]
USAN: Naloxone Hydrochloride
INN: Naloxone Hydrochloride [rINNM (en)]
INN: Hidrocloruro de naloxona [rINNM (es)]
INN: Naloxone, Chlorhydrate de [rINNM (fr)]
INN: Naloxoni Hydrochloridum [rINNM (la)]
INN: Налоксона Гидрохлорид [rINNM (ru)]
Chemical name: 17-Allyl-6-deoxy-7,8-dihydro-14-hydroxy-6-oxo-17-normorphine hydrochloride dihydrate; (-)-(5R,14S)-9a-Allyl-4,5-epoxy-3,14-dihydroxymorphinan-6-one hydrochloride dihydrate
Molecular formula: C19H21NO4,HCl,2H2O =399.9
CAS: 465-65-6 (naloxone); 357-08-4 (anhydrous naloxone hydrochloride); 51481-60-8 (naloxone hydrochloride dihydrate)
ATC code: V03AB15
Read code: y03KC

Chemical Structure of Naloxone

In Chin., Eur. (see ) ,Int.,Jpn,Pol.,and US. Forms specified may be anhydrous, dihydrate, or both.

Ph. Eur. 5.5 (Naloxone Hydrochloride Dihydrate; Naloxone Hydrochloride BP 2005). It contains two molecules of water of hydration. A white or almost white, hygroscopic, crystalline powder. Freely soluble in water; soluble in alcohol; practically insoluble in toluene. Store in airtight containers. Protect from light.

USP 29 (Naloxone Hydrochloride). It is anhydrous or contains two molecules of water of hydration. A white to slightly off-white powder. Soluble in water, in dilute acids, and in strong alkali; slightly soluble in alcohol; practically insoluble in chloroform and in ether. Its aqueous solution is acidic. Store in airtight containers at a temperature of 25 degrees, excursions permitted between 15 degrees and 30 degrees. Protect from light.

Physicochemical Characteristics
Infusions of naloxone hydrochloride should not be mixed with preparations containing bisulfite, metabisulfite, long-chain or high-molecular-weight anions, or solutions with an alkaline pH.

Adverse Effects
Nausea and vomiting have occurred with naloxone. Some adverse effects may be associated with opioid withdrawal. There have been individual reports of hypotension, hypertension, cardiac arrhythmias, and pulmonary oedema, generally in patients given naloxone postoperatively. Seizures have also been reported infrequently.

Hypertension,1,2 pulmonary oedema,3 and cardiac arrhythmias including ventricular tachycardia and fibrillation4 have been reported after the postoperative use of naloxone, generally in patients with pre-existing heart disease undergoing cardiac surgery. However, there have also been reports in healthy patients,5,6 including some fatalities.5

Hypotension, bradycardia, and precipitation of focal seizures have been reported in patients given high-dose naloxone for acute ischaemic stroke.7

Ventricular fibrillation has been observed in an opioid addict given naloxone to reverse the effects of diamorphine.8 However, this patient was later shown to have hepatic cirrhosis and alcoholic cardiomyopathy and the National Poisons Information Service in London noted that it had never been informed of such a suspected adverse reaction despite being contacted in about 800 cases of opioid poisoning each year.9 In a later report severe adverse effects were noted in 6 of 453 subjects given naloxone to reverse diamorphine intoxication.10 The effects were: asystole (1 case), generalised convulsions (3 cases), pulmonary oedema (1 case), and violent behaviour (1 case).

1. Tanaka GY. Hypertensive reaction to naloxone. JAMA 1974; 228: 25–6. PubMed
2. Azar I, Turndorf H. Severe hypertension and multiple atrial premature contractions following naloxone administration. Anesth Analg 1979; 58: 524–5. PubMed
3. Flacke JW, et al. Acute pulmonary edema following naloxone reversal of high-dose morphine anesthesia. Anesthesiology 1977; 47: 376–8. PubMed
4. Michaelis LL, et al. Ventricular irritability associated with the use of naloxone hydrochloride: two case reports and laboratory assessment of the effects of the drug on cardiac excitability. Ann Thorac Surg 1974; 18: 608–14. PubMed
5. Wride SRN, et al. A fatal case of pulmonary oedema in a healthy young male following naloxone administration. Anaesth Intensive Care 1989; 17: 374–7. PubMed
6. Taff RH. Pulmonary edema following naloxone administration in a patient without heart disease. Anesthesiology 1983; 59: 576–7. PubMed
7. Barsan WG, et al. Use of high dose naloxone in acute stroke: possible side effects. Crit Care Med 1989; 17: 762–7. PubMed
8. Cuss FM, et al. Cardiac arrest after reversal of effects of opiates with naloxone. BMJ 1984; 288: 363–4. PubMed
9. Barret L, et al. Cardiac arrest following naloxone. BMJ 1984; 288: 936. PubMed
10. Osterwalder JJ. Naloxone—for intoxications with intravenous heroin and heroin mixtures—harmless or hazardous? A prospective clinical study. Clin Toxicol 1996; 34: 409–16. PubMed
Naloxone should be used with caution in patients physically dependent on opioids, or who have received large doses of opioids, as an acute withdrawal syndrome may be precipitated (see Dependence and Withdrawal under Opioid Analgesics, ). Naloxone crosses the placenta and a withdrawal syndrome may be precipitated in neonates of opioid-dependent mothers.

Caution is required in patients with cardiac disease or those receiving cardiotoxic drugs.

The duration of action of some opioids exceeds that of naloxone; patients should therefore be carefully observed after administration in case of relapse.

Naloxone is absorbed from the gastrointestinal tract but it is subject to considerable first-pass metabolism. It is metabolised in the liver, mainly by glucuronide conjugation, and excreted in the urine. It has a plasma half-life of about 1 hour after parenteral administration. Naloxone crosses the placenta.

Pregnancy and the neonate.
A study in 30 mothers given a single intravenous dose of naloxone during the second stage of labour, indicated that naloxone rapidly crossed the placental barrier so that some therapeutic effect might be anticipated in most neonates.1 Placental transfer in 7 further mothers given naloxone intramuscularly was considered to be too variable for therapeutic purposes.

In 12 neonates given naloxone hydrochloride 35 or 70 micrograms intravenously via the umbilical vein, the mean plasma half-life was 3.53 or 2.65 hours respectively.2 These half-lives were 2 to 3 times longer than those reported for adults, possibly due to a diminished ability of the newborn to metabolise drugs by conjugation with glucuronic acid. Mean peak plasma concentrations of 8.2 nanograms/mL or 13.7 nanograms/mL in those given 35 or 70 micrograms respectively, were reached within 40 minutes but this time was very variable, and in 5 neonates peak concentrations were reached within 5 minutes. Naloxone hydrochloride 200 micrograms intramuscularly in 17 further neonates produced peak concentrations of 7.4 to 34.6 nanograms/mL at 0.5 to 2 hours.

1. Hibbard BM, et al Placental transfer of naloxone. Br J Anaesth 1986; 58: 45–8. PubMed
2. Moreland TA, et al Naloxone pharmacokinetics in the newborn. Br J Clin Pharmacol 1980; 9: 609–12. PubMed
Uses and Administration
Naloxone is a specific opioid antagonist that acts competitively at opioid receptors. It is an effective antagonist of opioids that possess agonist or mixed agonist-antagonist activity although larger doses may be needed for compounds with the latter activity. It is used to reverse opioid central depression, including respiratory depression, induced by natural or synthetic opioids in the treatment of known or suspected opioid overdosage, postoperatively after the use of opioids during surgery, and in neonates after the administration of opioid analgesics to the mother during labour.

Naloxone hydrochloride is usually given intravenously for a rapid onset of action, which occurs within 2 minutes. The onset of action is only slightly less rapid when it is given intramuscularly or subcutaneously. Other routes, including the endotracheal, have also been used. The duration of action of naloxone is dependent on the dose and route of administration; it is usually 1 to 4 hours but may be much shorter.

In the treatment of known or suspected opioid overdosage, the initial dose of naloxone hydrochloride is 0.4 to 2 mg given intravenously and repeated if necessary at intervals of 2 to 3 minutes. If no response has been observed after a total dose of 10 mg then the diagnosis of overdosage with drugs other than opioids should be considered. If the patient is suspected of being physically dependent on opioids the dose may be reduced to 100 to 200 micrograms to avoid precipitating withdrawal symptoms. In children, the usual initial dose is 10 micrograms/kg intravenously followed, if necessary, by a larger dose of 100 micrograms/kg (for an alternative children's dose suggested in the USA to treat opioid intoxication, see under Administration, ). In both adults and children, if the intravenous route is not feasible the intramuscular or subcutaneous route can be used.

Naloxone hydrochloride may also be used postoperatively to reverse central depression resulting from the use of opioids during surgery. For adults, a dose of 100 to 200 micrograms (1.5 to 3 micrograms/kg) may be given intravenously at intervals of at least 2 minutes, titrated for each patient in order to obtain an optimum respiratory response while maintaining adequate analgesia.

All patients receiving naloxone should be closely observed as the duration of action of many opioids exceeds that of naloxone and repeated doses by intravenous, intramuscular, or subcutaneous injection may be required. Alternatively, to sustain opioid antagonism, an intravenous infusion may be used. The manufacturer recommends naloxone hydrochloride 4 micrograms/mL in sodium chloride 0.9% or glucose 5%, infused at a rate titrated in accordance with the patient's response, both to the infusion and previous bolus injections; more concentrated solutions have also been used, and an infusion rate of 400 to 800 micrograms/hour has been suggested.

Opioid-induced depression in neonates resulting from the administration of opioid analgesics to the mother during labour may be reversed by giving naloxone hydrochloride 10 micrograms/kg to the infant by intravenous, intramuscular, or subcutaneous injection, repeated at intervals of 2 to 3 minutes if necessary. Alternatively, a single intramuscular dose of about 60 micrograms/kg may be given at birth for a more prolonged action. Naloxone should be given with caution to the infants of opioid dependent mothers since withdrawal symptoms can result.

Some opioid analgesics have been formulated with naloxone hydrochloride to reduce their potential for parenteral abuse. Naloxone hydrochloride has also been used cautiously in small doses to diagnose opioid dependence by precipitating the withdrawal syndrome (see and under Naltrexone, ).

Administration in infants and children.
The Committee on Drugs of the American Academy of Pediatrics1,2 has recommended a dose for naloxone of 100 micrograms/kg by intramuscular, intravenous, or intratracheal administration for neonates, including premature infants, to the age of 5 years or 20 kg body-weight for acute respiratory depression induced by opioids; absorption may be erratic after intramuscular use. Children over 5 years or 20 kg should be given a minimum of 2 mg. These doses may be repeated as necessary to maintain opioid reversal. The use of injections containing 20 micrograms/mL of naloxone hydrochloride is no longer recommended because of the fluid load involved at these doses, especially in small neonates.1,3 Lower initial doses of 10 micrograms/kg may be considered for other clinical situations such as respiratory depression during pain management.2

1. American Academy of Pediatrics. Emergency drug doses for infants and children and naloxone use in newborns: clarification. Pediatrics 1989; 83: 803. PubMed
2. Committee on Drugs. Drugs for pediatric emergencies. Abstract: Pediatrics 1998; 101: e13. PubMed Full version: online (accessed 30/06/06)
3. American Academy of Pediatrics. Naloxone dosage and route of administration for infants and children: addendum to emergency drug doses for infants and children. Pediatrics 1990; 86: 484–5. PubMed
Eating disorders.
Endogenous opioids may have a role in the pathophysiology of eating disorders,1 thus opioid antagonists such as naloxone and naltrexone have been tried in their management. However, their role appears to be limited and they do not form part of the usual management of these conditions.

1. de Zwaan M, Mitchell JE. Opiate antagonists and eating behavior in humans: a review. J Clin Pharmacol 1992; 32; 1060–72. PubMed
Non-opioid overdosage.
Naloxone antagonises the action of exogenous and endogenous opioids. This may explain the varying responses reported to naloxone used in the treatment of overdosage with non-opioids, some of which may modulate endogenous opioids.

Benefit has been reported1 with naloxone in valproate overdosage, although the evidence is based on case reports. There have also been case reports suggesting benefit in overdosage with camylofin,2 chlorpromazine,3 and ibuprofen.4 A study5 with midazolam in healthy subjects found that naloxone did not reverse respiratory depression, although there had been earlier reports of benefit in coma due to benzodiazepines.

Naloxone has been used for clonidine intoxication, but retrospective reviews6,7 have concluded that responses are inconsistent, and there have been reports of hypertension. A lack of response has also been reported8 in brimonidine overdosage. There has been a report9 of the successful use of naloxone after captopril overdosage.

Naloxone may also be of benefit in overdosage with drugs that are structurally related to opioids, including apomorphine,10 dextromethorphan,11 and loperamide.12

1. Roberge RJ, Francis EH. Use of naloxone in valproic acid overdose: case report and review. J Emerg Med 2002; 22: 67–70. PubMed
2. Schvartsman S, et al. Camylofin intoxication reversed by naloxone. Lancet 1988; ii: 1246. PubMed
3. Chandavasu O, Chatkupt S. Central nervous system depression from chlorpromazine poisoning: successful treatment with naloxone. J Pediatr 1985; 106: 515–6. PubMed
4. Easley RB, Altemeier WA. Central nervous system manifestations of an ibuprofen overdose reversed by naloxone. Pediatr Emerg Care 2000; 16: 39–41. PubMed
5. Forster A, et al. Respiratory depressant effects of different doses of midazolam and lack of reversal with naloxone—a double-blind randomized study. Anesth Analg 1983; 62: 920–4. PubMed
6. Fiser DH, et al. Critical care for clonidine poisoning in toddlers. Crit Care Med 1990; 18: 1124–8. PubMed
7. Wiley JF, et al. Clonidine poisoning in young children. J Pediatr 1990; 116: 654–8. PubMed
8. Sztajnbok J. Failure of naloxone to reverse brimonidine-induced coma in an infant. J Pediatr 2002; 140: 485–6. PubMed
9. Varon J, Duncan SR. Naloxone reversal of hypotension due to captopril overdose. Ann Emerg Med 1991; 20: 1125–7. PubMed
10. Bonuccelli U, et al. Naloxone partly counteracts apomorphine side effects. Clin Neuropharmacol 1991; 14: 442–9. PubMed
11. Schneider SM, et al. Dextromethorphan poisoning reversed by naloxone. Am J Emerg Med 1991; 9: 237–8. PubMed
12. Friedli G, Haenggeli C-A. Loperamide overdose managed by naloxone. Lancet 1980; i: 1413. PubMed
For reference to the use of opioid antagonists, including naloxone, in the management of pruritus, see under Nalmefene,

Reversal of opioid effects.
Naloxone is used postoperatively to reverse central depression resulting from the use of opioids during surgery. However, the beneficial analgesic effects of the opioids may also be reversed, and the increasing use of short-acting intravenous opioid analgesics should reduce the need for its use.

In patients receiving longer-term opioids, naloxone has been reported to alleviate some of their adverse effects without loss of therapeutic efficacy. Naloxone reversed respiratory depression in a patient given intrathecal morphine,1 and urinary retention in 3 patients after epidural morphine,2 without reversing analgesia. However, a study3 in patients receiving extradural fentanyl found that naloxone failed to relieve urinary retention whereas pain scores rapidly increased. Naloxone given intravenously has been shown to reverse the delay in gastric emptying induced by opioid analgesics in healthy subjects4 and in women during labour.5 Continuous intravenous infusion of naloxone reduced the incidence of adverse effects in patients receiving morphine by patient-controlled analgesia for postoperative pain.6 Pain control was not compromised and the lower dose of naloxone used (250 nanograms/kg hourly as opposed to 1 microgram/kg hourly) appeared to have an opioid-sparing effect. In patients receiving long-term opioids, oral naloxone in a daily dose equivalent to 20 to 40% of the daily opioid dose relieved opioid-induced constipation without compromising analgesic control.7,8 Doses equivalent to 10% or less of the opioid dose were ineffective.9 However, other studies10 have found adverse effects even at low doses of naloxone, and the optimum dose remains unclear. Methylnaltrexone, a related opioid antagonist that has fewer CNS effects, is also under investigation.11

1. Jones RDM, Jones JG. Intrathecal morphine: naloxone reverses respiratory depression but not analgesia. BMJ 1980; 281: 645–6. PubMed
2. Rawal N, et al. Naloxone reversal of urinary retention after epidural morphine. Lancet 1981; ii: 1411. PubMed
3. Wang J, et al. Low-dose naloxone in the treatment of urinary retention during extradural fentanyl causes excessive reversal of analgesia. Br J Anaesth 1998; 80: 565–6. PubMed
4. Nimmo WS, et al. Reversal of narcotic-induced delay in gastric emptying and paracetamol absorption by naloxone. BMJ 1979; 2: 1189. PubMed
5. Frame WT, et al. Effect of naloxone on gastric emptying during labour. Br J Anaesth 1984; 56: 263–5. PubMed
6. Gan TJ, et al. Opioid-sparing effects of a low-dose infusion of naloxone in patient-administered morphine sulfate. Anesthesiology 1997; 87: 1075–81. PubMed
7. Sykes NP. Oral naloxone in opioid-associated constipation. Lancet 1991; 337: 1475. PubMed
8. Sykes NP. Oral naloxone in opioid-associated constipation. Lancet 1991; 338: 582.
9. Robinson BA, et al. Oral naloxone in opioid-associated constipation. Lancet 1991; 338: 581–2. PubMed
10. Thomas MC, Erstad BL. Safety of enteral naloxone and i.v. neostigmine when used to relieve constipation. Am J Health-Syst Pharm 2003; 60: 1264–7. PubMed
11. Foss JF. A review of the potential role of methylnaltrexone in opioid bowel dysfunction. Am J Surg 2001; 182: (5A suppl): 19S–26S. PubMed
Diagnostic use.
Naloxone is used to reverse opioid effects in the diagnosis of opioid overdose, although some workers have recommended that it should only be used in patients with clinical signs of opioid overdose.1

Naloxone has also been used in the diagnosis of opioid dependence. It has been given intravenously to precipitate withdrawal symptoms, but methods that do not induce acute withdrawal have also been investigated. Pupillary dilatation in response to topical naloxone solution has been suggested as a useful method, but varying results have been reported depending on the strength of the solution used. A study2 using naloxone hydrochloride solution 1 mg/mL distinguished patients with a physical dependence from non-dependent patients who had received opioids on a single occasion as pre-operative medication, but this response was not confirmed in another study3 using naloxone 400 micrograms/mL solution. Another study4 reported that a 2 mg/mL solution of naloxone hydrochloride gave useful results in an outpatient setting. However, there has been a report5 of withdrawal syndrome and pupillary dilatation in 4 opioid dependent subjects after instillation of naloxone solution 40 mg/mL.

1. Hoffman JR, et al. The empiric use of naloxone in patients with altered mental status: a reappraisal. Ann Emerg Med 1991; 20: 246–52. PubMed
2. Creighton FJ, Ghodse AH. Naloxone applied to conjunctiva as a test for physical opiate dependence. Lancet 1989; i: 748–50. PubMed
3. Loimer N, et al. Conjunctival naloxone is no decision aid in opioid addiction. Lancet 1990; 335: 1107–8. PubMed
4. Ghodse AH, et al. Evaluation of the opioid addiction test in an out-patient drug dependency unit. Br J Psychiatry 1999; 175: 158–62. PubMed
5. Sanchez-Ramos JR, Senay EC. Ophthalmic naloxone elicits abstinence in opioid-dependent subjects. Br J Addict 1987; 82: 313–15. PubMed
Opioid overdosage.
Naloxone is usually given intravenously in opioid overdosage but may also be given intramuscularly if intravenous access is not available. Alternative routes have also been tried; a study1 using intranasal naloxone found that it was effective for prehospital management of suspected opioid overdosage, although response was slower than with intramuscular injection.

1. Kelly A-M, et al. Randomised trial of intranasal versus intramuscular naloxone in prehospital treatment for suspected opioid overdose. Med J Aust 2005; 182: 24–7. PubMed
Endogenous opioids may have a role in the pathophysiology of shock but studies investigating naloxone for the treatment of shock have produced contradictory results. A systematic review1 concluded that naloxone does increase blood pressure in various forms of shock, but no significant effect on mortality was shown. The US manufacturers have noted that the optimal dose and duration of therapy with naloxone have not been established, and that caution should be exercised before its use, particularly in patients with underlying pain or who have previously received opioids and may have developed opioid tolerance.

1. Boeuf B, et al. Naloxone for shock. Available in The Cochrane Database of Systematic Reviews; Issue 3. Chichester: John Wiley; 2003 (accessed 04/10/05). PubMed

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Re: subotex=suboxone

Post by Red_Bull » Sun Mar 03, 2013 12:01 pm

A evo gledam ovaj forum i po prvi put se javljam nego ranije nisam htjeo da se jvaljam sta znam ima dosta razloga iz kojih nisam htjeo da pisem nego da neduzim. Vidim da se vodi rasprava o suboxonu i koje kakvih komentara . . . Evo do sada ga ja koristim vec 2 god redovno a pijem 3 tablete i sta znam kako na koga utice meni je legao dobro. Nego prije nego cu preci na suboxon pio sam 20 tableta heptanona i na detoksu sam bio pa sam se prebacio na sub.Mogu vam reci da dosta raje nemoze da se navikne na sub dosta raje je dozivljavalo neke napade itd.Dobijam tablete za 15 dana tako da nisam obavezan da idem na terapiju svaki dan a hocu ovu da istaknem ko god kaze da se nemoze na njega uzet heroin laze ! ! !

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Re: subotex=suboxone

Post by sanela » Sun Mar 03, 2013 2:23 pm

@RedBull, dobrodošao na forum :)
Samo nešto mi je upalo u oko u tvom postu
Dobijam tablete za 15 dana tako da nisam obavezan da idem na terapiju svaki dan a hocu ovu da istaknem ko god kaze da se nemoze na njega uzet heroin laze ! ! !
Pa me zanima da li ti supstituciju koristiš za liječenje ili za drogiranje? Odnosno, da li ti koristiš suboxon da se pika da si na liječenju, a svako malo se "počastiš" heroinom?
Na drugoj temi si napisao da si bio u tri komune, a u jednoj 26 mjeseci, pa si sad na supstituciji. Kako gledaš na iskustvo koje si stekao u komunama?

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Re: subotex=suboxone

Post by Red_Bull » Tue Mar 12, 2013 11:24 am

SANELA DOK SE MALO SNADEM KAKO DA KORISTIM SAJT PA CE MI BOLJE ICI ;) Evo ovako iskreno da kazem sto se tice Suboxona meni pase kao lijek a potrudit cu se da napisem nesto o tome sta mislim povodom boravka u komunama te i o lijecenju sto suboxonom , heptanonom itd . Vrlo mlad sam zapao u ovaj svijet sa nekih 14 god sada imam 28 i previse me je zivot slomio u ovom razdoblju ma da covijek da me sretne na ulici nikada nebi rekao da sam bio ili mozda sam trenutno.Upravo moram da idem na kontrolu ( testiranje ) pa cu malo pokusati napisati naredni put i iskreno se nadam da ce nekom pomoci ;)

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Re: subotex=suboxone

Post by Red_Bull » Mon Mar 18, 2013 1:24 pm

Pa evo da iznesem sta mislim povodom komuna.Ovako moje misljenje je da covijek moze da dosta toga nauci u komuni prvenstveno osebi sto i jeste bitno.Komunu nemoze svako da zavrsi jer nije to bas tako kako ljudi pricaju odes u komunu malo kopas kanale i sta ti ja znam budes neki odredeni period i zavrsis te tu da je kraj tvojoj borbi o ovisnosti.Nemojte se zavaravati jer to nije tako ama ni blizu.Svakom bi preporucio da ne ide u komunu radi nekog drugog i necega jer bezveze traci svoje vrijeme a i ljudi oko sebe.Ja u prve dvije komune nisam usppjeo da izdrzim a to su bile Aleksandrovac-Marijanovac kod Banja Luke te Bastasi kod Banja Luke dok sam zavrsio program kod Kaknja u komuni UG PROI.Mislim da su u principu male razlike oko izbora komuna u biti sve se svodi na spoznaju sebe svojih vrlina , mana te uzroka pocetka drogiranja naravno da se svaki sticenik obraduje u raznim fazama tako da ako se neko odluci na taj korak neka se prepusti programu date komune.Ja se nisam prepustao pa sam nesto htjeo da mjenjam nesto ne sto je manipulacija samog sebe.Moram da kkazem da sam stvarno imao dosta teskih trenutaka pri boravcima u komunama mimo toga sto nisam otisao navucen pa eto ako odete navuceni bice vam jos duplo teze e ko voli neka izvoli !Trenutno sam na SUBOXON terapiji i moram da kazem da sam zadovoljan sa lijekom jer znam dosta slucajeva u kojim ljudima neodgovara subox.Necu da lazem s vremena na vrijeme se zdrmam samo DOPOM ali se ne dovodim u situacije da zaredam po nekoliko dana mada imam para ali iz dosadasnjeg izkustva znam sebe dovoljno i kako sam se dovodio u razne nezgodne pozicije kada bi bilo koju supstancu zaredao po par dana cak i sedmica.Barem ja sam covijek megaloman sto se tice droge dok tu isto bi dodao da ima i do ljudske psihe pa opet sve zavisi od covijeka do covijeka.Ovaj subox pijem vec 2 god tako da sam ustalio svoju terapiju i hvala bogu nemam problema mislim da je cudan jer do sada sto sam god probao da koristim za suzbijanje DOPA nije imalo efekta te sam konacno se namjerio na ovaj lijek sto nemora da bude u drugim slucajevima.Imao bi jos dosta toga da napisem ali nesto mi se neda pa eto ako sam barem nekom malo pomogao sa ovim svojim tekstom drago mi je.Sta koga zanima slobodno nneka pita a ja cu se potruditi dati svoje misljenje i odgovor.

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Re: subotex=suboxone

Post by tix » Sat Jun 22, 2013 12:46 pm

...ja ne kužim samo zašto to meni ne sam ovisnik i otišao u komuni na 3,5 godine....vratio se i 8 godina bio čist...dok se nisam jednom puknuo i tad mi je bilo ok jer sam se brzo skinu sa subovima i to bez problema...sad opet mi se desilo da zadnjih mjesec dana rokam po dopu, ali razlika je u tome što se ne mogu skinuti više...izludim...pustim da prođe i 14-16 sati od zadnjeg uzimanja (znači stvaRNO TE POČNE ROKATI KRIZA)...uzmem sub(znači poslije 14 - 16 sati) i opere me takva nervoza, znojenje, grčevi u trbuhu i sve te poznate stvari...i naravno idem ga probijati...i tako već 5- 6 puta i nikako se ne uspijem razumijem zašto na mene tako reagira suboxsone poslije toliko sati????? a netko ga može uzeti nakon 6 -7 sati i skinut će mu krizu....meni je samo pojača!!!!!!
MOLIM neki savjet jer ću opet otići u kurac a to ne želim!!!!!

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Re: subotex=suboxone

Post by Lujka » Sat Jun 22, 2013 1:00 pm sam ovisnik..

Zaboravi prošlo svršeno vrijeme, i dalje si ovisnik :cry:
Postoje stvari koje su poznate i one koje to nisu, između njih nalaze se vrata.

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Re: subotex=suboxone

Post by tix » Sat Jun 22, 2013 1:24 pm

Lujka sam ovisnik..

Zaboravi prošlo svršeno vrijeme, i dalje si ovisnik :cry:
...nažalost imaš pravo... :( :( :(...a daj mi reci jel ima kakva kombinacija da si olakšam samo taj prvi dan kad uzmem sub...jer stvarno pustim da prođem 14 - 16 sati od zadnjeg uzimanja dopa, da me skroz kriza zašora i onda ga stavim pod jezik i sve se pojača još jaće umjesto da mi pomogne...a ne želim hepove uzimati

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