A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Oxycontin Side Effects, and Drug Interactions - Oxycodone HCl
Oxycontin Side Effects, and Drug Interactions - Oxycodone HCl
SIDE EFFECTS
The safety of OxyContin® was evaluated in double-blind clinical
trials involving 713 patients with moderate to severe pain of various
etiologies. In open-label studies of cancer pain, 187 patients received
OxyContin® in total daily doses ranging from 20 mg to 640 mg
per day. The average total daily dose was approximately 105 mg per day.
Serious adverse reactions which may be associated with OxyContin®
(oxycodone hydrochloride controlled-release) tablet therapy in clinical
use are those observed with other opioid analgesics, including respiratory
depression, apnea, respiratory arrest, and (to an even lesser degree)
circulatory depression, hypotension, or shock (see OVERDOSAGE).
The non-serious adverse events seen on initiation of therapy with OxyContin®
are typical opioid side effects. These events are dose-dependent, and
their frequency depends upon the dose, the clinical setting, the patient’s
level of opioid tolerance, and host factors specific to the individual.
They should be expected and managed as a part of opioid analgesia.
The most frequent (>5%) include: constipation, nausea, somnolence,
dizziness, vomiting, pruritus, headache, dry mouth, sweating, and asthenia.
In many cases the frequency of these events during initiation of therapy
may be minimized by careful individualization of starting dosage, slow
titration, and the avoidance of large swings in the plasma concentrations
of the opioid. Many of these adverse events will cease or decrease in
intensity as OxyContin® therapy is continued and some degree
of tolerance is developed.
Clinical trials comparing OxyContin® with immediate-release
oxycodone and placebo revealed a similar adverse event profile between
OxyContin® and immediate-release oxycodone. The most common
adverse events (>5%) reported by patients at least once during therapy
were:
| Table 3 |
| Adverse Events |
OxyContin® |
Immediate-Release |
Placebo |
| (n=227) |
(n=225) |
(n=45) |
| (%) |
(%) |
(%) |
| Constipation |
23 |
26 |
7 |
| Nausea |
23 |
27 |
11 |
| Somnolence |
23 |
24 |
4 |
| Dizziness |
13 |
16 |
9 |
| Pruritus |
13 |
12 |
2 |
| Vomiting |
12 |
14 |
7 |
| Headache |
7 |
8 |
7 |
| Dry Mouth |
6 |
7 |
2 |
| Asthenia |
6 |
7 |
- |
| Sweating |
5 |
6 |
2 |
The following adverse experiences were reported in OxyContin®
treated patients with an incidence between 1% and 5%.
In descending order of frequency they were anorexia, nervousness, insomnia,
fever, confusion, diarrhea, abdominal pain, dyspepsia, rash, anxiety,
euphoria, dyspnea, postural hypotension, chills, twitching, gastritis,
abnormal dreams, thought abnormalities, and hiccups.
The following adverse reactions occurred in less than 1% of patients
involved in clinical trials or were reported in post marketing experience:
General: accidental injury, chest pain, facial edema, malaise,
neck pain, pain.
Cardiovascular: migraine, syncope, vasodilation, ST depression.
Digestive: dysphagia, eructation, flatulence, gastrointestinal
disorder, increased appetite, nausea and vomiting, stomatitis, ileus.
Hemic and Lymphatic: lymphadenopathy.
Metabolic and Nutritional: dehydration, edema, hyponatremia,
peripheral edema, syndrome of inappropriate antidiuretic hormone secretion,
thirst.
Nervous: abnormal gait, agitation, amnesia, depersonalization,
depression, emotional lability, hallucination, hyperkinesia, hypesthesia,
hypotonia, malaise, paresthesia, seizures, speech disorder, stupor, tinnitus,
tremor, vertigo, withdrawal syndrome with or without seizures.
Respiratory: cough increased, pharyngitis, voice alteration.
Skin: dry skin, exfoliative dermatitis, urticaria.
Special Senses: abnormal vision, taste perversion.
Urogenital: amenorrhea, decreased libido, dysuria, hematuria,
impotence, polyuria, urinary retention, urination impaired.
DRUG INTERACTIONS
Opioid analgesics, including OxyContin®, may enhance the neuromuscular
blocking action of skeletal muscle relaxants and produce an increased
degree of respiratory depression.
Oxycodone is metabolized in part to oxymorphone via cytochrome P450 2D6.
While this pathway may be blocked by a variety of drugs (e.g., certain
cardiovascular drugs including amiodarone and quinidine as well as polycyclic
antidepressants), such blockade has not yet been shown to be of clinical
significance with this agent. Clinicians should be aware of this possible
interaction, however.
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