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Desomorphine (Dihydrodesoxymorphine) is an abbreviated name of 4,5-epoxy-17- methylmorphinan-3-ol. It is a semisynthetic analog of morphine and an agonist of opioid receptors, in which the 6-hydroxyl group and the carbon bond (in 7 and 8) are reducted. Desomorphine contains an ether bridge between two rings R4 and R5 through an oxygen group, contains a hydroxy group bound to R3 and a methyl group on the nitrogen atom by R17. It is different from morphine because of the absence of a secondary hydroxy group in R6. It exists in four isoforms: A,B, C and D, the last two isoforms are mainly used, D- most often. Desomorphine is most often produced from over-the-counter medicine or prescription medicine, mixed with ethyl alcohol, gasoline, red phosphorus, iodine, hydrochloric acid and paint thinner. The substance itself was first described by Small in 1932, and introduced in Switzerland in 1940 by Hoffmann - La Roche under the trade name Permonid. It was initially available as a hydrobromide salt, but its use was discontinued in 1952. Dangerous effects of the substance are associated with its home production, low degree of purification, high-availability and low price. It is known that it is 5 times cheaper than heroin in the USA. This fact allows the users to avoid interactions with dealers and police. Desomorphine is a colorless, well-crystallized organic base, similar to morphine and other alkaloids. It has a molar mass of 271.35 g/mol, a melting point of 189 degrees Celsius and a pKa value of 9.69. Desomorphine passes the brain-blood barrier, binding to the opioid receptors similar to the pharmacokinetic distribution of all alkaloids of phenanthrene structure. Moreover, it is poorly-soluble in water at room temperature in the form of a free base (solubility about 1.425 mg/l). But in allotropic forms (which are often used recreationally) it is solved better in water, acetone, ethyl acetate and alcohol.

Pharmacokinetics and pharmacodynamics.
The main metabolic pathway of the first phase is carried out mainly by cytochrome p450 CYP3A4, but other forms of cytochrome are also involved: CYP2C18 and CYP2C8, are partially involved in the stages of the first phase. The main metabolic reactions are: N-demethylation, hydroxylation, N-oxidation. In the second phase, desomorphine undergoes glucuronidation and sulfation, and the enzymes involved in this process are as follows: UGT1A1, UGT1A8, UGT1A9, UGT1A10, UGT2B4, UGT1A3, UGT2B7, UGT2B15 and UGT2B17, which produce desomorphine glucoronide. Several metabolites of desomorphine are described: nordesomorphine, desomorphine-N-oxide, norhydroxydesomorphine and 5 hydroxylated metabolites, which have no practical significance. At the same time, 3A4 is solely responsible for the formation of levorphanol-N-oxide. Desomorphine is an agonist of μ- and δ – opioid receptors. Thus, it causes pronounced tolerance, addiction and withdrawal syndrome. Norhydroxydesomorphine is identified exclusively during the first 20-30 minutes, after that, it cannot be detected by in vivo mass spectrometry. Tolerance to desomorphine is developed due to rapid internalization stimulated by phosphorylation of the carboxyl-terminal cytoplasmic domain of the receptor. Addiction is developed almost instantly after the first or the second use. Higher analgesic potential (compared to other opiates) is associated with the presence of a phenolic group at C3, able of participating in the weak interaction of the hydrogen bond with the opioid receptor. In addition, the loss of the C6-OH group increases pharmacological activity due to the absence of a double bond between C7 and C8 (which is present in morphine and codeine). The phenolic group B C3 plays an important role in pharmacological activity, just like the C6H group, which increases lipophilicity of desomorphine. According to the results of the research, it was revealed that desomorphine has 10 times effects that of morphine and is 3-4 times more toxic. Half-lethal dose of desomorphine in mice is 27 mg/kg. Sedative effect is the most dominant among other effects of desomorphine. After intravenous administration, it has fast (almost instant) start of action. Analgesic effect of the substance is 8-10 times higher than that of morphine, however it involves a high risk of respiratory depression development, it is associated with earlier withdrawal syndrome(as it was mentioned above). The most common undesirable effects of desomorphine are: miosis, hyperemia, paresthesia, constipation, urinary retention, nausea, vomiting, often provokes allergic reactions and seizures, respiratory depression, which can lead to death. The absence of a hydroxyl group in the substance and its replacement with hydrogen, followed by an increase in lipophilicity, may explain the higher toxicity of this substance compared to morphine. There is also high occurrence of convulsions. Moreover, desomorphine is a cholinesterase inhibitor, which leads to seizures and other neurological symptoms.


Clinical effects of desomorphine.
After desomorphine administration, as well as the other psychoactive substances of this group, reproduction of clinical effects in order of the rate of interaction of the main active substance with opioid receptors occurs. So, first effects manifest immediately after intravenous administration. Initially pronounced sedation and euphoria occur, lasting from ten minutes to a couple of hours with a decrease in intensity of the effects. These clinical symptoms are considered positive desirable effects. Also, cognitive euphoria, reduction of anxiety, Dream potentiation effect, Internal hallucination, which are usually present after administration of a high dose in case there is no tolerance.

As for negative undesirable effects, after desomorphine intake there are: constipation, decreased appetite up to its complete absence, impaired focusing of the vision with a spasm of accommodation and the occurrence of "double vision", nausea and vomiting, respiratory depression - a decrease in the frequency of respiratory movements up to complete respiratory arrest, which is called opioid-induced respiratory depression, associated with a decrease in central reactivity to CO2, leading to hypoventilation, an increase in the partial pressure of carbon dioxide in arterial blood, which, in patients with depressed consciousness, causes asphyxia, with a decrease in the tone of the respiratory tract, redness of the skin (and the appearance of other local inflammatory changes or allergic reactions), decreased libido, impaired urination, decreased cough reflex, the development of physical and mental dependence, decreased heart rate and blood pressure.

Gastrointestinal effects are associated with the effect of desomorphine on the μ and σ-receptors. There is a decrease in gastrointestinal peristalsis, deterioration of digestive reflux, a decrease in bile secretion, pancreatic and intestinal secretions. Gastric congestion can last up to 12 hours. An increase in the tone of the Oddi sphincter leads to an increase in pressure in the biliary tract, up to the level of pressure in the intestine. The most typical symptoms are nausea and vomiting, which can lead to aspiration complications. In people with chronic drug use, constipation is described, sometimes leading to obstruction.

Most often, in acute severe opiate poisoning, hypoxia is complex in nature, characterized by disruption of almost all links of oxygen transport. Thus, the most frequent and severe manifestation of acute opiate poisoning is the development of mixed hypoxia caused by hypoxic hypoxia due to respiratory disorders, circulatory hypoxia as a result of disorders of general and regional blood circulation and microcirculation, hemic and secondary tissue hypoxia. Ultimately, hypoxia is the leading factor in various metabolic disorders that manifest themselves at the cellular, subcellular and molecular levels.

Any enteral method of desomorphine administration is not used due to the ineffectiveness and impossibility of achieving the necessary effects, minimal bioavailability and pronounced instant side effects that "overlap" the desired positive effects in severity (as a rule, side effects develop immediately after oral or intrarectal use and are mainly realized in the form of local foci of reactive inflammation of the mucous membrane, the occurrence of gastrointestinal symptoms). The most common method of administration is intravenous. The dose depends on the saturation of the prepared solution, the quantitative and qualitative composition of the components included and varies from 0.03 to 0.08 mg / kg, while 0.08 mg / kg is a high dose limit, and implies a high risk of severe side effects.


Special instructions, interactions with other psychoactive substances.
The joint use of desomorphine (as well as other opioid receptor agonists) with psychostimulants in small doses does not cause critical conditions if opiates are used first. However, with each following increase in the dose, myocardial ischemia disproportionately occurs due to the resulting vasospasm with reflex bradycardia (which, in turn, is a complete decompensation of the heart, which can lead to negative cardiovascular events up to a disorder of atrioventricular conduction and acute coronary syndrome).

The combination of desomorphine and alcohol is dangerous. Thus, both substances are potentiating negative effects (mainly sedative, emetic, ataxic), which can eventually lead to serious consequences, ranging from transient disturbances of consciousness (up to coma), ending with a fatal outcome due to obstruction of the respiratory tract by vomit or respiratory arrest of central genesis.

The most dangerous combinations of desomorphine, in addition to alcohol, are combinations with GHB, GBL, ketamine, tramadol and MXE due to the increased depressive effect on the central nervous system, as well as an increase in cardiac conduction disorders risk, pressure overload of the heart, hypercapnia and respiratory distress syndrome. As for benzodiazepines and neuroleptics, when used together with desomorphine, in addition to the high risk of impaired consciousness, there is a danger of an excessive miotic effect, as well as sedative and analgesic effects. There are also several cases of myoclonus described.

MAO inhibitors and phenothiazine derivatives cause negative cardiovascular complications. The analgetic and hypotensive effects increase, the risk of respiratory depression increases up to complete respiratory arrest. Inducers of microsomal oxidation during systemic use (including barbiturates and carbamazepine) reduce the analgetic effect of desomorphine, and also lead to the development of cross-tolerance. NK1 receptor antagonists currently represent a new generation of antiemetics that can be used for treatment and prevention of nausea and vomiting when using desomorphine, instead of metoclopramide. Combinations of antiemetics can be more effective than monotherapy. Prevention of vomiting by a combination of a 5HT3-receptor antagonist and dexamethasone is preferable. With prolonged use of desomorphine, the main central complications developing are: tolerance, neurotoxicity and opioid-induced hyperalgesia. A specific clinical presentation includes hyperalgesia, myoclonus, allodynia and transistor or permanent confusion, and is an indication for preventive pharmacological therapy.

The classic presentation of an opiate overdose (without taking into consideration the severity and stages)
1. Impaired consciousness (any stage of stunning or coma).
2. Excessive constriction of the pupils (persistent miosis), a decrease in their reaction to light, ptosis, nystagmus and convergence insufficiency.
3. Muscle hypotension and a decrease in the tendon reflex (sometimes there may be muscle hypertonus).
4. Reduction or absence of pain sensitivity.
5. Reduction of the frequency of respiratory movements to 12-10 per minute, or respiratory arrest.

First aid algorithm for overdose:
1. If a person is unconscious or has impaired consciousness of any stage, call paramedics (911) or one more person to help.
2. If the person is not breathing, is unconscious and has no pulse, it is mandatory to clean the oral cavity of foreign bodies (remove false teeth, teeth, mucus, vomit) and start resuscitation measures with indirect heart massage and artificial respiration in compliance with hygiene rules.
3. If there is naloxone, inject 2 mg intranasally or 0.4 mg intramuscularly. After two minutes, you should repeat the administration of a dose of 0.4 mg until the effect appears. If the person reacts to stimuli in any way – carry out intensive stimulation of consciousness and breathing (up to pain irritation). At the same time, you should monitor the person's condition.
4. Implement the algorithm before the arrival of paramedics.

Toxicology of desomorphine.
Addicts more frequently administer “Krokodil” orally, subcutaneously, or intravenously, the intravenous way being the most used by users of this drug. The effects are observed very quickly, approximately 15–30 s after the intravenous injection and approximately 3–5 min for the subcutaneous administration. As noted above, the active substance of “Krokodil” is desomorphine, and through the intravenous use of “Krokodil,” other highly toxic components of this drug can enter the bloodstream along with desomorphine. Then, intravenous injection of homemade and street “Krokodil” can cause several pathologies, such as coronary artery burst, septicemia, and other systemic damage due to infections, such as pneumonia and meningitis. In addition, infections by HIV and hepatitis A, B, and C are reported in “Krokodil” addicts using contaminated needles. These viruses may cause systemic damage, especially HIV, which causes several complications in the immune system. The incidence of hepatitis C (HCV) is very high, while HIV prevalence is significantly lower. A possible explanation for this fact is that the acidity of the street and homemade drug solutions can render HIV inactive when stored in syringes, while such inactivation of HCV would require higher concentrations of acid or longer exposure times. Another effect that can be observed in users of “Krokodil” is due to unsanitary conditions in the preparation of this drug; it is common for users to develop infections such as methicillin-resistant Staphylococcus aureus.

In fact because “Krokodil” is routinely injected with little or no purification, it can cause immediate skin irritation and ulcers, destruction of skin and severe muscle, and cartilage tissue damage. However, demonstrated that the lesions observed after “Krokodil” exposure can include several parts of the body that are not typically used as sites for injecting drugs. This suggests that the ill effects of “Krokodil” are not limited to localized injuries, but spread throughout the body, with neurological, endocrine, and organ damage associated with chemicals common to “Krokodil” production. These alterations consist of motor and speech impairments, memory and personality changes, thyroid abnormalities, and liver and kidney damage. In addition, Lemon (2013) describes the use of homemade “Krokodil” as a possible cause of hallucinations. Because “Krokodil” presents an analgesic effect, the user often fails to recognize immediately these deleterious consequences.


In relation to impurities observed in the production of “Krokodil,” several toxic effects are observed due to orange-colored liquid contaminated with various toxic and corrosive by products or residuals like organic solvents (gasoline, ethyl acetate, or paint thinner), as well as hydrochloric acid, iodine, and red phosphorus. According to, iodine excess is associated with damage to the endocrine system and muscles. Moreover, jaw osteonecrosis develops as a complication in patients who use “Krokodil” and one of the main causes of jaw osteonecrosis is exposure to phosphorus compounds. This pathology is a painful condition characterized by avascular necrosis of bone in the oral cavity that is commonly associated with localized swelling and, sometimes, purulent discharge. The presence of gasoline and hydrochloric acid in the production of “Krokodil” can contribute to the local damage induced by this drug, causing skin irritation, ulcers, and thrombophlebitis. In addition, chronic exposure to gasoline and paint thinner may cause encephalopathy and neurological damage. Moreover, it is known that lead exposure induces hematological, renal, and hepatic damage in the human body. In addition, this heavy metal can affect the hippocampus, causing memory and learning impairment and induce reproductive disorders in the human body.

Local toxic effects: abscesses, gangrene, thrombophlebitis, limb ulceration and amputations, jaw osteonecrosis, skin discoloration, black and open ulcers, necrosis, skin and soft tissue infection, necrosis, bleeding, rotting gums and ears, scabs, popped skin lesions.
Systemic toxic effects: blood vessel, muscle, cartilage and bone damages, multiple organ failure, hypothyroidism, liver and kidney inflammation, pain, swelling, endocarditis, pneumonia, meningitis, pale skin, low blood pressure and heart beats, swollen hands, death.
Neurotoxicity: loss of cognitive functions, speech difficulty and changes of personality, loss of memory, hallucinations.

Hydriodic acid and red phosphorous are known to be very corrosive and dangerous substances, especially when administered intravenously. The formation of white phosphorus is perhaps another plausible explanation for the observed tissue damage. Nevertheless, the production of white phosphorus from red allotropic modification in an acidic and warm media in the presence of hydriodic acid and red phosphorus must still be confirmed. Moreover, a different crystal form of phosphorus (dark red needles) is obtained when red phosphorus is submitted to iodine recrystallization at low temperatures. This indicates that some modifications may occur on the red phosphorus molecules during krokodil preparation. Red phosphorus is the reagent of the formation of the hydriodic acid, which is the main responsible for the reaction to form desomorphine. However, large amounts of phosphorous are used and it is not totally consume during the reaction. This is an ineffective purification process, and therefore it is expected to have phosphorus in the krokodil. Moreover, red phosphorous have been suggested to induce permanent deformities in the facial skull, such as the appearance of jaw osteonecrosis. The exact mechanism is unknown but apoptosis of osteoclasts, disturbance of osteoclast progenitor cell differentiation, disturbance of osteoclast enzyme activity, destruction of bone microstructure caused by phosphorous deposition and antineovascularization have been suggested. Although there are available phosphorus coatings from matchbox strikers (i.e. ‘‘safe matches’’) without oxidizers, they are more expensive and not commonly used for ‘‘krokodil’’ synthesis. Besides the reported toxic effects for users, those that only produce ‘‘krokodil’’ are also at risk due to gas iodine production during the heating process of the synthesis. Indeed, iodine excess is associated with damage to the endocrine system and muscles.

Finally, chronic exposure to remnants of the solvents such as gasoline (including lead and/or other additives) or paint thinner and the alkaline drain cleaner used in codeine extraction may cause encephalopathy and neurological damage. Lead exposure induces neurologic and hematological dysfunctions (due to its capacity to inhibit zinc-containing enzymes), renal and hepatic damage as well as reproductive disorders in the human body. The neurologic action of lead damages cells in the hippocampus, a part of the brain involved in memory and interferes with the release of neurotransmitters, especially glutamate, which is the responsible for many functions including learning.​
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