Dehace retard
Dehace retard Uses, Dosage, Side Effects, Food Interaction and all others data.
Dehace retard is an opioid analgesic used as an alternative or adjunct to codeine to treat moderate to severe pain, severe dyspnea, and cough.
It is semi-synthetic, and was developed in Germany in 1908 during an international search to find a more effective antitussive agent to help reduce the spread of airborne infectious diseases such as tuburculosis. It was marketed in 1911.
Possible opioid related side effects include, but are not limited to, drowsiness, nausea, headache, dry mouth, constipation, difficulty passing urine, and mild euphoria.
| Trade Name | Dehace retard |
| Generic | Dihydrocodeine |
| Dihydrocodeine Other Names | Dihydrocodeine |
| Type | |
| Formula | C18H23NO3 |
| Weight | Average: 301.3801 Monoisotopic: 301.167793607 |
| Groups | Approved, Illicit |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | Austria |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Dehace retard is an opioid analgesic agent used for the management of pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate.
Dehace retard is used for the treatment of moderate to severe pain, including post-operative and dental pain [2]. It can also be used to treat chronic pain [1], breathlessness and coughing.
In heroin addicts, dihydrocodeine has been used as a substitute drug, in doses up to 2500mg/day to treat addiction. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014322/]
Dehace retard is also used to associated treatment for these conditions: Severe Pain, Moderate Pain
How Dehace retard works
Dehace retard is metabolized to dihydromorphine -- a highly active metabolite with a high affinity for mu opioid receptors. [3]
Food Interaction
- Avoid alcohol. Alcohol can enhance the CNS depressant effects of this drug.
Volume of Distribution
The disposition of dihydrocodeine is described as a two compartment model. [2]
Elimination Route
Bioavailability is low (approximately 20%) if administered orally. This may be due to poor gastrointestinal absorption. It is also likely due to pre-systemic metabolism by the liver and intestinal wall. [2]
The AUCs after oral and intravenous administration are similar (3203ug/l/h and 3401ug/l/h, respectively). [2]
Time to peak values are 1.6 and 1.8hours for a 30mg and 60mg dose, respectively. The concentrations achieved were 71.8 ug/1 and 146 ug/1, respectively. [2]
Half Life
4h
Clearance
Plasma clearance is approximately 300ml/min. [2]
The pharmacokinetics of dihydrocodeine and active metabolite dihydromorphine have been reported to be linear. [1]
The decline in plasma dihydrocodeine concentrations after intravenous administration has been described as bi-exponential, with a sleep decline in the initial 2h following administration, followed by a mono-exponential decline thereafter. Clearance was not dose dependent. [2]
Elimination Route
Renal elimination and urinary excretion. [1]
Innovators Monograph
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