It can also interact with certain supplements. Different interactions can cause different effects. For instance, some interactions can interfere with how well a drug works.
Other interactions can increase side effects or make them more severe. Below are lists of medications that can interact with Cymbalta. Before taking Cymbalta, talk with your doctor and pharmacist. Tell them about all prescription, over-the-counter, and other drugs you take.
Also tell them about any vitamins, herbs, and supplements you use. Sharing this information can help you avoid potential interactions. If you have questions about drug interactions that may affect you, ask your doctor or pharmacist. Cymbalta can increase serotonin levels in your body. Using Cymbalta with other drugs that also increase serotonin may raise your risk for serotonin syndrome.
Serotonin syndrome is a rare but potentially life threatening condition. Taking multiple medications that increase serotonin levels could cause serotonin to build up to dangerous levels in your blood. Before taking Cymbalta, be sure to tell your doctor if you take any of the medications listed above. They may want to monitor you for any signs of serotonin syndrome. Or they may have you take a different drug to treat your condition.
Taking Cymbalta with these drugs may increase Cymbalta levels in your body. Slowing down this process could raise your risk for side effects from Cymbalta. Certain drugs have stronger effects on these enzymes. Examples of strong CYP1A2 inhibitors include:. Examples of CYP2D6 inhibitors include:. Before you take Cymbalta, be sure to tell your doctor if you take any of these medications.
They can determine which drug is the best fit for you. This means it can affect the levels of other drugs that are also broken down by this enzyme. However, some medications can cause side effects if their levels in your body are changed slightly. Examples of these drugs include:. Before taking Cymbalta, talk with your doctor about all the medications you take. They can determine whether Cymbalta can be taken with your other medications.
Drugs that affect serotonin levels, such as Cymbalta, may increase your risk for bleeding. Before taking Cymbalta, tell your doctor if you take any of the medications listed above. This monitoring may include ordering blood tests. Or they may decide to use a different medication to treat your condition. This is an herb that can be used to treat depression. Cymbalta can raise your serotonin levels.
Because St. If you have any questions about eating certain foods with Cymbalta, talk with your doctor. Clinical studies of the drug have shown that taking it the month before delivery may increase the risk of severe bleeding immediately afterward postpartum hemorrhage.
The manufacturer of Cymbalta maintains a pregnancy registry. The registry tracks the results of pregnant people taking the drug. You can join this registry online or by calling You should also tell your doctor right away if you become pregnant while taking this drug. You can take Cymbalta at any time of the day. However, you should try to take it around the same time every day.
This helps make sure you have a consistent amount of the drug in your body. The best time for you to take Cymbalta may depend on what you use the drug for and how often you take it each day.
Your doctor can help you decide the best time for you to take Cymbalta. Doing so may affect how well your body absorbs the drug. This could raise your risk for side effects or make the drug less effective. You can also call the American Association of Poison Control Centers at or use their online tool. But if your symptoms are severe, call or your local emergency number, or go to the nearest emergency room right away.
As with all medications, the cost of Cymbalta can vary. To find current prices for Cymbalta in your area, check out GoodRx. The cost you find on GoodRx. Before approving coverage for Cymbalta, your insurance company may require you to get prior authorization. This means that your doctor and insurance company will need to communicate about your prescription before the insurance company will cover the drug. The insurance company will review the prior authorization request and decide if the drug will be covered.
If you need financial support to pay for Cymbalta, or if you need help understanding your insurance coverage, help is available. Cymbalta is available in a generic form called duloxetine.
And generics tend to cost less than brand-name drugs. To find out how the cost of duloxetine compares to the cost of Cymbalta, visit GoodRx. They may have a preference for one version or the other. If you have questions about using other drugs with Cymbalta, talk with your doctor or pharmacist.
They can review your medications and discuss treatment options with you. Cymbalta may cause harm to a fetus. However, more research is needed in this area. However, there have been a few reports of drowsiness, poor feeding , and trouble gaining weight in infants exposed to breast milk containing duloxetine.
Duloxetine is the active drug in Cymbalta. If you choose to breastfeed while taking Cymbalta, you should watch for any trouble feeding or drowsiness in your child. Together, you can weigh the risks and benefits of breastfeeding while taking the drug and discuss your other treatment and feeding options. This drug has a boxed warning. A boxed warning alerts doctors and patients about drug effects that may be dangerous.
Clinical studies have shown antidepressants such as Cymbalta increase the risk of suicidal thoughts and behaviors in children and young adults ages 24 years or younger. In people ages 65 and older, antidepressants can actually reduce this risk. Before taking Cymbalta, talk with your doctor about your health history. Cymbalta may not be right for you if you have certain medical conditions or other factors affecting your health.
These include:. When you get Cymbalta from the pharmacy, the pharmacist will add an expiration date to the label on the bottle. This date is typically 1 year from the date they dispensed the medication. The expiration date helps guarantee that the medication is effective during this time.
If you have unused medication that has gone past the expiration date, talk to your pharmacist about whether you might still be able to use it. How long a medication remains good can depend on many factors, including how and where you store the medication.
Avoid storing this medication in areas where it could get damp or wet, such as bathrooms. This helps prevent others, including children and pets, from taking the drug by accident. It also helps keep the drug from harming the environment. This article provides several useful tips on medication disposal. You can also ask your pharmacist for information on how to dispose of your medication.
Cymbalta capsules are available in three strengths: 20 milligrams mg , 30 mg, and 60 mg. It can be taken with or without food. The exact mechanism by which Cymbalta treats MDD, GAD, diabetic neuropathy, fibromyalgia, and chronic musculoskeletal pain is not known. Cymbalta is classified as a serotonin-norepinephrine reuptake inhibitor SNRI. The active drug ingredient in Cymbalta, duloxetine, inhibits neuronal serotonin and norepinephrine reuptake. To a lesser extent, duloxetine also inhibits dopamine reuptake.
The effect of this on drug interactions is unknown. Food delays the time it takes for duloxetine to reach peak concentration, from 6 hours to 10 hours. However, this has no overall effect on maximum concentrations. Do not start Cymbalta in patients treated with MAOIs , including linezolid and intravenous methylene blue.
This can increase the risk of serotonin syndrome. Cymbalta is contraindicated for 14 days after stopping an MAOI intended to treat a psychiatric disorder.
Counsel Cymbalta users that treatment should not be stopped without talking with their prescriber. Cymbalta should be gradually tapered to avoid discontinuation syndrome. If someone experiences withdrawal symptoms during their Cymbalta taper, consider returning to the previously prescribed dose. Once withdrawal symptoms subside, the taper can be continued at a more gradual rate. Disclaimer: Medical News Today has made every effort to make certain that all information is factually correct, comprehensive, and up to date.
However, this article should not be used as a substitute for the knowledge and expertise of a licensed healthcare professional.
You should always consult your doctor or other healthcare professional before taking any medication. The drug information contained herein is subject to change and is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. The absence of warnings or other information for a given drug does not indicate that the drug or drug combination is safe, effective, or appropriate for all patients or all specific uses.
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Find out how foods and…. Cymbalta duloxetine. Medically reviewed by Dena Westphalen, Pharm. What is Cymbalta? Moreover, the vagueness of this complaint is also something they will likely capitalize upon. To be sure, there are distinct types of pain —e. Cymbalta is looking to capture part of that market. The analgesic mechanism of Cymbalta is as with much in psychiatry unknown. Some have argued it works by relieving the depression and anxiety experienced by patients in pain.
Click on the figure above for other potential mechanisms, from a recent article by Dharmshaktu et al. But the more important question is: does it work? The evidence for musculoskeletal pain is less convincing. The effects were not tremendous, even though they were statistically significant see example above, click to enlarge. In other words, it sounds like the FDA really wanted to get Cymbalta in the hands of more patients and more doctors.
These include pain intensity, patient ratings of overall improvement, physical functioning, and mental functioning. This review comprised the side-by-side analyses of 12 double-blind, placebo-controlled trials of duloxetine in patients with chronic pain diabetic peripheral neuropathic pain, fibromyalgia, chronic pain due to osteoarthritis, and chronic low back pain. Average pain reduction was assessed over 3 months as the primary efficacy outcome.
Other measures used were physical function and Patient Global Impression of Improvement. In 10 of the 12 studies, statistically significant greater pain reduction was observed for duloxetine- compared with placebo-treated patients. The response rates based on average pain reduction, improvement of physical function, and global impression were comparable across all 4 chronic pain states.
The analyses reported here show that duloxetine is efficacious in treating chronic pain as demonstrated by significant improvement in pain intensity, physical functioning, and patient ratings of overall improvement. The prevalence of chronic pain in the United States and Europe has been estimated at Pain represents the most common reason for patients to seek medical counsel [ 4 ].
Many types of pain, including chronic pain, affecting different patient populations elderly, children, minorities, substance abusers remain undertreated [ 5 , 6 ], and a complete resolution of pain is rarely achieved [ 7 ]. Untreated or undertreated pain has significant physical, psychological, social, and financial consequences [ 8 ].
Unlike acute nociceptive pain, chronic pain is a pathological state associated with functional and structural changes within the peripheral and central nervous systems. Among these changes, central sensitization and impairment of associated pain inhibitory circuits have been extensively researched [ 9 - 12 ]. These pathophysiological mechanisms are involved in and at least partially responsible for the development and maintenance of chronic pain states, regardless of their respective underlying etiologies e.
Three main categories of chronic pain are typically recognized [ 13 ]. These include neuropathic pain resulting from nerve damage or dysfunction either in the peripheral or in the central nervous system, e. Chronic pain conditions such as chronic low back pain CLBP may result from a number of causes, which can technically fall into any of these 3 chronic pain categories just discussed. Serotonin 5-HT and norepinephrine NE have been implicated in the mediation of endogenous pain inhibitory mechanisms via the descending pain inhibitory pathways in the brain and spinal cord [ 12 , 14 , 15 ].
In chronic pain states, the net inhibitory effect of these monoamines is postulated to be reduced or lost; consequently, shifting the descending pain modulatory system from a state of inhibition towards a state of pain facilitation [ 16 , 17 ].
Preclinical studies have shown that duloxetine effectively reduces pain behavior across a range of persistent, neuropathic, and inflammatory pain models [ 19 - 21 ], in a dose range that is consistent with inhibition of 5-HT and NE reuptake. Thus, the analgesic effect of duloxetine is believed to result from increased activity of 5-HT and NE within the CNS [ 18 , 20 , 21 ], presumably either by enhancing descending pain inhibitory pathways in the brain and spinal cord or other unknown CNS actions.
Irrespective of the underlying pathology or its absence, pain sensation becomes maladaptive, pathological, and enhanced, at least partly, due to the imbalance between excitatory and inhibitory pathways within the CNS. In previously published clinical trials, duloxetine has been shown to be effective in treating patients with DPNP [ 22 - 24 ] and FM [ 25 - 28 ]. Safety and tolerability of duloxetine has been described previously and will not be addressed here in the individual publications cited above, and articles with a focus on safety [ 34 - 42 ].
The trials were of at least week duration and evaluated duloxetine doses of mg to mg daily. Several of the studies in FM were of 6-month duration, but for comparison purposes only 3-month data are presented here.
Details about the inclusion and exclusion criteria for each of the chronic pain states are provided in the published manuscripts for the individual studies [ 22 - 28 , 30 , 32 , 43 ]. All of the studies required that patients have a hour average pain rating of 4 or greater based on an point numerical rating scale at study entry and have chronic pain for at least 3 to 6 months prior to study entry. Patients were excluded if they had any serious medical or psychiatric condition that could compromise their participation in the study.
All protocols excluded patients with clinically significant impairment in mental function. Patients with major depressive disorder were excluded from all studies except those in FM. The primary efficacy measure in all studies was the hour average pain rating rating scale ranging from 0 [no pain] to 10 [worst possible pain].
The benchmarks used to assess the clinical importance of changes in some of the above measures were based on the recommendations of the IMMPACT consensus on the clinical significance of change across pain states [ 33 ]. One point decrease in BPI physical interference is considered clinically important. All analyses were conducted on an intent-to-treat ITT basis.
Treatment effects were evaluated based on 2-sided tests with a significance level of 0. No adjustments were made for multiple comparisons. When an average score was computed from individual items, it was calculated from nonmissing values. For all analyses, baseline refers to the last nonmissing observation at or before the random assignment visit and endpoint refers to the last nonmissing observation in the 3-month treatment phase [last observation carried forward LOCF ].
For continuous variables, an analysis of covariance ANCOVA model was used including baseline value, treatment, and investigator. For time-to-first-response analysis, the Kaplan-Meier survival estimate was calculated by treatment group at each time point Week 1 to Week Patients who did not meet response criteria were considered as right-censored observation a data point is above a certain value but it is unknown by how much.
Treatment difference was assessed through log-rank test. SAS version 9 was used to perform all statistical analyses. In the 2 remaining studies, duloxetine was numerically better than placebo. The observed baseline pain severity across the studies was approximately 6. On average, duloxetine-treated patients reported pain reduction of Duloxetine hydrochloride is a selective dual 5-HT and NE reuptake inhibitor with central analgesic properties.
Preclinically, duloxetine is efficacious in models of persistent, inflammatory, and neuropathic pain [ 19 - 21 ], suggesting that it may be efficacious in the treatment of chronic pain conditions in which central sensitization is believed to be one of the underlying pathophysiological mechanisms [ 50 , 51 ]. Central sensitization is dependent upon the activation of a descending pain facilitatory pathway originating in the brainstem [ 52 ].
Duloxetine, by enhancing monoaminergic tone, may potentially reduce the consequences of central sensitization by shifting the descending pain modulatory pathway from a state of facilitation to a state of inhibition [ 16 , 17 ]. Consistent with the preclinical data, duloxetine, has demonstrated remarkable consistency of analgesic effect across all 3 main categories of chronic pain.
Duloxetine-treated patients demonstrated a significantly greater pain reduction compared with placebo-treated patients in 10 of the 12 studies and a numerically greater reduction in the remaining 2 studies. Patients receiving duloxetine for the treatment of chronic pain states had significantly higher response rates corresponding to clinically moderate and substantially important improvement compared with patients receiving placebo.
A previous report by Farrar et al. Duloxetine-treated patients demonstrated significant improvement in physical functioning in 8 of the 12 studies. Regardless of the measures used in these studies, patients with chronic pain had a significant improvement in overall physical functioning. There was also a significant overall improvement in duloxetine-treated patients as demonstrated by the PGI-improvement rating a measure of the degree of change at the time of assessment. The time-to-response data demonstrated that there was a significant separation between duloxetine and placebo at 1 to 2 weeks for 9 of the 12 studies and at Day 21 for the remaining 3 studies.
The limitations to this work should be noted.
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