Mobic vs meloxicam: Meloxicam vs Ibuprofen, what’s the difference?
Meloxicam vs Ibuprofen, what’s the difference?
Medically reviewed by Carmen Pope, BPharm. Last updated on Aug 23, 2022.
The main differences between meloxicam and ibuprofen are:
- Meloxicam is considered a stronger medicine than ibuprofen
- Meloxicam is only available on prescription and ibuprofen is available over the counter as well as on prescription
- Meloxicam is a long-acting medicine that only needs to be given once a day. Ibuprofen in its usual form needs to be given three to four times a day, although extended-release forms of ibuprofen that last 12 to 24 hours are available
- Ibuprofen is FDA approved to treat most mild-to-moderate painful conditions, such as toothache, back pain, and primary dysmenorrhea, as well as pain or inflammation caused by arthritis. Meloxicam is only approved to treat pain or inflammation caused by arthritis
- The risk of gastrointestinal disturbances (such as gastric ulcers) and cardiovascular events (such as heart attacks) appears higher with meloxicam compared to ibuprofen.
Both meloxicam and ibuprofen belong to the class of medicines known as nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by blocking enzymes that make prostaglandins, which are substances that contribute to inflammation and pain. Taking an NSAID such as ibuprofen or meloxicam reduces inflammation and pain.
What is meloxicam?
Meloxicam is the generic name for Mobic. It is an NSAID that is mainly used to treat pain from arthritis and is available by prescription as an oral 7.5 mg tablet, 10 mg tablet, and 7.5 mg/5 mL oral suspension.
The usual dosage is 7.5mg once daily although this dosage can depend on your condition and your doctor’s instructions. Maximum concentrations are reached five to six hours after a dose, and its duration of pain relief can be up to 24 hours. It is metabolized in the liver and excreted by the kidneys, and is available as a generic.
Meloxicam is not available in combination with other medicines.
What is ibuprofen?
Ibuprofen is the generic name for Advil or Motrin.
It is a widely used and prescribed NSAID that is also available over the counter.
The usual dosage is 200mg to 400mg (1 to 2 tablets or capsules) every 4 to 6 hours, with a maximum of 1200mg (6 tablets or capsule) in 24 hours, unless your doctor has told you otherwise. There are also longer-lasting forms of ibuprofen available which only need to be taken once or twice a day.
Ibuprofen is also available in combination with other medicines such as diphenhydramine (Advil PM). Like meloxicam, ibuprofen is metabolized in the liver and excreted by the kidneys, and is available as a generic.
Does meloxicam have more side effects than ibuprofen?
Because meloxicam and ibuprofen are both NSAIDs, they have similar side effects, which may include abdominal pain, constipation, diarrhea, heartburn, nausea, tinnitus, and a rash.
All NSAIDs carry a risk of cardiovascular disease, including an increased risk for blood clots, stroke, or a heart attack; however, the risk with meloxicam appears higher than with ibuprofen (only applies to ibuprofen dosages less than 3200mg/day).
Meloxicam is also more likely than ibuprofen to cause gastrointestinal (GI) disturbances, such as gastric bleeding and ulceration. Consuming more than three alcoholic beverages per day while taking any NSAID increases the risk of GI disturbances.
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Meloxicam vs Mobic Comparison – Drugs.
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May also be
prescribed off label for Fibromyalgia, Inflammatory Conditions, Tendonitis.
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Mobic may also be used for purposes not listed in this comparison guide.
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Do not drink alcohol while taking…** The Controlled Substances Act (CSA) schedule information displayed applies to substances regulated under federal law.
There may be variations in CSA schedules between individual states.
Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.
Medical Disclaimer
“golden mean” of non-steroidal anti-inflammatory drugs
Rapid and most complete pain relief is one of the priorities of medical care. Pain is the most unpleasant manifestation of the main pathological conditions, so its effective suppression can significantly improve the quality of life of patients and gain their confidence, which is important when it comes to the onset of a chronic disease requiring long-term pathogenetic therapy.
Pain therapy is of fundamental importance in musculoskeletal diseases such as osteoarthritis (OA) and low back pain (LBP), which are currently associated with most cases of chronic non-cancer pain [1-3].
From the point of view of medical science, chronic pain is a serious and independent threat to the patient’s life.
Persistent severe pain determines the negative changes in homeostasis, mediated by the reaction of the sympathetic-adrenal system – an increase in blood pressure and heart rate, as well as procoagulative changes in the blood coagulation system. These changes lead to a significant increase in the risk of developing dangerous cardiovascular complications (CVS) [1, 2].
In such nosological forms as OA and chronic LBP, which are not accompanied by visceral pathology, but are characterized by severe pain that often persists for months and years, the risk of developing fatal CVCs is significantly increased [1, 2].
This statement is confirmed by a study by Swiss scientists E. Nüesch et al. [4], who assessed the frequency of deaths in 1163 patients with OA with a follow-up period of about 5 years. According to the data obtained, the risk of death due to CVD in patients suffering from this “non-fatal” disease is 1.7 times higher than in the general population. In the course of the subsequent analysis, the scientists identified the only factor that was clearly associated with the development of fatal CVCs in patients with OA – a pronounced dysfunction of the joints, preventing normal movement.
Among the dead, such disorders were observed in 35%, while among the survivors – only 17% ( p <0.001) [4].
Similar results are presented by Japanese researchers M. Tsuboi et al. [5], who observed the dynamics of the state in 944 patients with various rheumatic diseases for 10 years. It was found that in patients with gonarthrosis the risk of death from CVE is more than 2 times higher than in the population (odds ratio – OR – 2.32).
The work of Australian scientists K. Zhu et al. [6], who followed a group of 1484 elderly women (over 70 years of age) with chronic LBP for 5 years. Among them, 21.7% initially and 26.9% at the end of the observation period experienced pain daily. In this subgroup, the risk of death from CVE was more than 2 times higher (relative risk – RR 2.13 at 95% confidence interval – CI – from 1.35 to 3.34) than in the group of patients who had less pain .
It is impossible not to note one more, purely practical aspect of the problem of adequate anesthesia.
Patients come to the doctor’s office primarily for relief of suffering; “understanding” the situation, finding out the exact diagnosis is a secondary, although undoubtedly important, goal of seeking medical help. Excessive enthusiasm for diagnostic measures and “basic” means to the detriment of simple and effective methods of pain control can cause a negative attitude of the patient towards the attending physician and turn him away from the methods of classical medicine. On the contrary, the effective elimination of the most painful symptoms will be the most effective way to win the patient’s trust and achieve strict adherence to a complex scheme of long-term pathogenetic therapy [1, 2].
However, effective control of chronic pain is not easy. An illustration of this is the work of the Spanish scientists L. Arboleya et al. [7], who assessed the opinion on the results of treatment of 897 patients with OA who received analgesics for at least 6 months, most often non-steroidal anti-inflammatory drugs (NSAIDs): diclofenac, aceclofenac and piroxicam.
46% of the respondents were dissatisfied with the effect of prescribed drugs, and only 1 patient out of 6 considered himself completely satisfied with the result of analgesic therapy.
In this regard, the data of British researchers M. Gore et al. [8], who evaluated the practice of prescribing analgesics (paracetamol, NSAIDs, tramadol, “weak” and “strong” opioids) in patients with OA and LBP. For various reasons – due to inefficiency, adverse events, etc., during the 1st month of treatment, prescribed drugs were canceled in almost 90% of patients (from 30 to 60% were cases of replacement therapy, up to 15% – its increase – the use of various combinations). It can be seen that in most cases (not less than ⅔), the analgesic drug initially recommended by the doctor did not justify hopes and did not become a solution to the pain problem [8].
It should be remembered that the development of pain, especially chronic pain, is a complex, multicomponent pathological process.
Its development involves local inflammation, muscle spasm, damage to the elements of the ligamentous apparatus, biomechanical disorders, dysfunction of the pain system (peripheral and central sensitization, “exhaustion” of antinociceptive mechanisms, etc.) [1, 2, 9, 10]. It is obvious that monotherapy, even with the most effective means, cannot always ensure therapeutic success. Only an integrated approach based on the combined use of drugs with different mechanisms of action can achieve effective control of chronic pain (Table 1) .
First-line pharmacotherapy for musculoskeletal pain is undoubtedly NSAIDs. They have a unique combination of analgesic, anti-inflammatory and antipyretic effects, providing effective relief of the main symptoms associated with the pathology of the OPS organs [1-3].
The main mechanism of the pharmacological action of NSAIDs is associated with the blockade of cyclooxygenase-2 (COX-2), which is formed in the foci of tissue damage and is responsible for the active synthesis of prostaglandins (PG) – the most important mediators of pain and inflammation.
It is important to note that the analgesic effect of NSAIDs is realized not only by reducing the excitability of peripheral pain receptors. Probably no less important is the effect of NSAIDs on the central mechanisms of pain formation – the phenomenon of central sensitization, which is also mediated by hyperproduction of PG (aseptic neuronal inflammation) and activation of glial cells that occur in response to persistent and powerful pain stimulation of the structures of the nociceptive system [1-3 ].
Obviously, if inflammation plays an important role in the pathogenesis of acute or chronic pain (even subclinical, as in OA and dorsalgia), accompanied by active synthesis of biologically active substances such as interleukins 1 and 6, tumor necrosis factor, the use of NSAIDs will be appropriate and necessary . Moreover, in this situation, as the data of many clinical studies show, in terms of their therapeutic activity, NSAIDs have a clear advantage over other analgesics – paracetamol and opioids, which do not have anti-inflammatory properties [1-3].
The therapist has an exceptional variety of NSAIDs in his arsenal. This creates difficulties for practitioners, because even experts cannot always determine the criteria for the merit of drugs that should be used to decide on the choice of one or another NSAID. The situation is further complicated by the active advertising activities of some manufacturing companies promoting their product as “the most effective and safe among all possible.” However, real practice clearly shows that none of the NSAIDs can be considered the best, and if the drug has an advantage in any parameter, it is likely that it will also have certain disadvantages.
The analgesic effect of all NSAIDs when used in therapeutic doses is practically the same. At least there is no conclusive data obtained in the course of a series of methodically correctly organized clinical trials that any drug from this group is significantly superior to others in analgesic action. The main difference between NSAIDs (sometimes very significant) is determined by their safety [3].
Among NSAIDs, two polar groups are distinguished, differing in their selectivity for COX-2 (their main pharmacological “target”): non-selective (n-NSAIDs) and highly selective – “coxibs”. The selectivity of NSAIDs avoids the suppression of the activity of the biochemical “brother” of COX-2 – the COX-1 enzyme, the work of which is extremely important for maintaining many vital functions, such as the protective properties of the mucous membrane (CO) of the gastrointestinal tract (GIT). The blockade of COX-1 (characteristic of n-NSAIDs) leads to a significant increase in the risk of developing severe, life-threatening gastrointestinal pathology (gastropathy and enteropathy associated with NSAIDs – NSAID gastropathy and NSAID enteropathy. In this regard, “coxibs” are much less dangerous [3 ].
However, selective suppression of COX-2 (without affecting COX-1) can lead to an imbalance in the synthesis of thromboxane A2 and prostacyclin, which increases the risk of vascular thrombosis.
In patients with cardiovascular diseases, this is fraught with an increased risk of developing severe CV events – myocardial infarction (MI) and ischemic stroke [3]. As can be seen, the use of n-NSAIDs and “coxibs” has serious limitations: they are not suitable for all patients (Table 2) . Accordingly, two main scenarios can be presented in which the use of representatives of these drug groups is most appropriate.
Thus, “coxibs” are more suitable for relatively young patients who need short-term analgesic therapy and have a moderate risk of developing complications in the form of organic and functional disorders of the gastrointestinal tract in the absence of severe concomitant CVS pathology.
n-NSAIDs (except for ketorolac, suitable only for short-term use) are more acceptable for patients of the older age group with a moderate risk of developing CVC, but without significant risk factors for developing NSAID gastropathy. In most cases, these drugs can only be used in combination with a gastroprotector (proton pump inhibitor).
A position between n-NSAIDs and “coxibs” should be assigned to drugs with moderate selectivity for COX-2. Their use should lead to a smaller number of pronounced complications in the form of organic and functional disorders of the gastrointestinal tract, but not be accompanied by a significant increase in the risk of developing CVS. This is a kind of “golden mean”, which is acceptable for most patients and is especially interesting now, when the medical community, after the bad memory of the “coxibs crisis”, is very wary of highly selective COX-2 inhibitors. At the same time, the problem of NSAID gastropathy, which is so characteristic of n-NSAIDs, will never lose its relevance.
In the mid-1990s, this position was occupied by diclofenac. However, at present, this drug no longer meets the high requirements of safe pharmacotherapy. In our country, primarily due to the widespread use of cheap generics of this drug, it is with diclofenac that the greatest number of complications in the form of organic and functional disorders of the gastrointestinal tract are associated [11].
The situation with the MTR is even worse. Thus, according to a meta-analysis conducted by P. McGettigan and D. Henry [12], (30 case-control studies, including 184 946 patients with CVD and 21 cohort studies, a total of > 2.7 million individuals), the risk of MI increases with the use of diclofenac by approximately 40% (OR 1.4). In a population study by Danish scientists E. Fosbøl et al. [13], taking diclofenac was accompanied by the highest risk of developing myocardial infarction, stroke, and death from CVD among NSAIDs, higher than that of coxibs.
Significantly more interest is attracted by another representative of the “golden mean” – a moderately selective COX-2 inhibitor meloxicam, which appeared in 1995 g. Since then, this effective and fairly safe drug remains one of the most popular representatives of the NSAID group, which is actively used in almost all countries of the world.
Meloxicam has been extensively tested in a large number of clinical trials; its effectiveness has been studied in a wide range of diseases and pathological conditions, ranging from anesthetic practice to chronic joint diseases.
These studies clearly confirmed that meloxicam is in no way inferior in its therapeutic potential to the “traditional” NSAIDs in the most common diseases characterized by musculoskeletal pain (OA, LBP, rheumatoid arthritis – RA and ankylosing spondylitis – AS) [14-22].
However, the main advantage of meloxicam is its good tolerability. In a series of large randomized clinical trials (RCTs), a significantly lower number of complications in the form of organic and functional disorders of the gastrointestinal tract was unambiguously confirmed when using this drug compared to n-NSAIDs.
The 4-week MELISSA study ( n =9323) compared meloxicam 7.5 mg with diclofenac 100 mg/day. The total number of side effects in the form of organic and functional disorders of the gastrointestinal tract when using meloxicam was significantly less – 13.3% versus 18.7% in the diclofenac group. At the same time, the number of episodes of discontinuation of therapy due to complications in patients treated with meloxicam was 2 times less: 3 and 6.
1%, respectively ( p <0.001). Dangerous complications - clinically pronounced ulcers, gastrointestinal bleeding (GI) and perforation while taking meloxicam were also less common (but not significant) - 5 and 7 cases, respectively [23].
A SELECT RCT ( n = 8656) was conducted in a similar manner, but piroxicam 20 mg was used as a comparison. This study showed a significant advantage of meloxicam in relation to the risk of developing severe complications in the form of organic and functional disorders of the gastrointestinal tract, which occurred in 7 and 16 patients, respectively ( p <0.05). As in the RCT MELISSA, dyspepsia and associated episodes of discontinuation of therapy were significantly more common in patients treated with the comparator drug: 10.3 and 3.8% versus 15.4 and 5.3%, respectively ( p <0.001) [ 24].
D. Yocum et al. [25] 774 patients with OA received meloxicam at a dose of 3.75, 7.5 and 15 mg, diclofenac 100 mg or placebo for 3 months.
The results of the study showed that the total number of complications in the form of organic and functional disorders of the gastrointestinal tract while taking meloxicam was significantly less than when using diclofenac – 19and 28%, respectively ( p <0.05).
The safety of meloxicam has also been confirmed in a number of cohort studies, such as H. Zeidler et al. [26]. This study involved 2155 German doctors who observed 13,307 rheumatological patients who received meloxicam at a dose of 7.5 mg (65%) or 15 mg (33%) for 1-3 months. The efficacy and tolerability of the drug was assessed by analyzing the data provided by the attending physicians in the relevant questionnaires. Although the majority of patients were over 60 years old, and 12% had a history of ulcers, undesirable effects in the form of organic and functional disorders of the gastrointestinal tract were noted in 0.8%, and pronounced ones – only in 5 patients (4 uncomplicated gastric ulcers and 1 perforation) [26 ].
Somewhat earlier P. Schoenfeld et al. [27] conducted a meta-analysis of 12 RCTs lasting from 1 to 24 weeks, comparing meloxicam with diclofenac, piroxicam, and naproxen in patients with OA, RA, and dorsalgia. It was shown that taking meloxicam was associated with a significantly lower total number of complications in the form of organic and functional disorders of the gastrointestinal tract (RR 0.64 at 95% CI from 0.59 to 0.69), the incidence of dyspepsia (OR 0.73 at 95% CI from 0.64 to 0.84), symptomatic ulcers, GI and perforations (OR 0.52 at 95% CI from 0.28 to 0.96), as well as the risk of discontinuation of therapy due to complications in the form of organic and functional disorders of the gastrointestinal tract (OR 0.59 at 95% CI from 0.52 to 0.67).
A later meta-analysis by G. Singh [25], which included data from 28 RCTs (24,196 patients), also confirms the higher safety of meloxicam at a dose of 7.5 mg compared to traditional NSAIDs in relation to the gastrointestinal tract.
Thus, the frequency of gastrointestinal bleeding when using this dose of meloxicam was only 0.03% (when taking 15 mg 0.2%), while in those receiving diclofenac at a dose of 100-150 mg / day – 0.15% [28].
In order to study the effect of meloxicam on the upper gastrointestinal tract, several years ago we conducted a retrospective analysis of the development of gastric and/or duodenal ulcers in rheumatological patients who were in 2002-2005. on inpatient treatment at the clinic of the FGBU NIIR RAMS. The studied groups consisted of persons who underwent esophagogastroduodenoscopy during this period for various reasons: 425 patients who received meloxicam, and 2428 – diclofenac (Fig. 1) . Figure 1. Detection of ulcers and multiple (> 10) erosions of the stomach and / or duodenal ulcer in patients who regularly received meloxicam or diclofenac [29]. In patients taking meloxicam, ulcers occurred almost 2 times less often, including patients with such a risk factor as an ulcer history [29].
In recent years, the problem of the negative effects of NSAIDs on the distal gastrointestinal tract has attracted much attention of researchers and practitioners. First of all, we are talking about NSAID enteropathy – a pathology of the small intestine (TC), which is accompanied by an increase in its permeability and the development of chronic inflammation associated with the penetration of bacteria or their components contained in the chyme into the intestinal wall. This complication can manifest itself as severe GI bleeding, perforation and strictures of the TC; however, its most characteristic symptom is subclinical blood loss leading to the development of chronic iron deficiency anemia (IDA) [3, 30, 31]. Recently, interest in this pathology has been very high, since even in the absence of life-threatening complications, NSAID enteropathy can have a significant negative impact on the patient’s health. After all, chronic IDA determines a significant decrease in the oxygen capacity of the blood, a decrease in resistance to stress and, ultimately, an increase in the risk of developing severe CVD.
This is confirmed by the work of G. Sands et al., published in 2012. [32]. The researchers conducted a meta-analysis of 51 RCTs comparing the safety of celecoxib and n-NSAIDs ( n = 50,116) to determine the relationship between reduced hemoglobin levels and the incidence of life-threatening systemic complications. It turned out that anemia dramatically increased the risk of developing severe CVD. Thus, in 932 patients who developed a clinically significant decrease in hemoglobin levels (more than 20 g/l), the incidence of MI was 0.6%, while in patients who did not have signs of anemia, it was only 0.2%. Similarly, the progression of coronary heart disease (CHD) was observed in 1.2 and 0.3% of patients [32].
NSAID enteropathy is a problem characteristic of “traditional” NSAIDs. There is strong evidence that c-NSAIDs (“coxibs”) are significantly safer than “traditional” NSAIDs in terms of the risk of developing this pathology [3].
The most modern technique for accurately diagnosing pathology of the mucous membrane of the jejunum and ileum, which occurs while taking NSAIDs, is video capsule endoscopy (VCE).
It was she who was used in a number of studies that compared the effect of “coxibs” and n-NSAIDs on the state of TC [3, 33].
In recent years, the first reports of a relatively low incidence of NSAID enteropathy with the use of meloxicam have appeared, confirmed by TBEV data. Thus, we recently conducted a study on the effect of meloxicam (Movalis) and diclofenac on the state of TC in 15 patients with AS. The choice of this nosological form for studying the development of NSAID enteropathy was not accidental. Patients with AS have an increased risk of developing TC pathology – there is a known association between chronic inflammatory bowel diseases and seronegative spondylitis. In addition, patients with AS often take NSAIDs, often for a long time and in high doses [34].
According to the results obtained, certain changes in the SO TC – the presence of inflammation, hemorrhages, erosions or ulcers were detected equally often while taking meloxicam 15 mg / day or diclofenac 100-200 mg / day: 71.
4 and 75%, respectively. However, the average number of erosions was significantly less in those who received movalis: 6.2±4.7 and 9.4±7.3, respectively [34].
Our data are consistent with those of Y. Maehata et al. [35]. They performed VCE in 29 volunteers with initially normal SO TC who received meloxicam 10 mg/day or celecoxib 200 mg/day for 2 weeks. The number of persons who, after a course of NSAIDs, had a pathology of the TC, when using meloxicam, was less than when taking “coxib” – 26.7 and 42.9% respectively.
It can be stated that, in relation to CVR, meloxicam is at least no worse than “traditional” NSAIDs. So, in a series of RCTs conducted in the late 90s of the XX century, it was shown that the risk of developing severe CV events when using meloxicam does not exceed that against placebo.
According to the results of the meta-analysis of 28 RCTs conducted by G. Singh [28], the incidence of myocardial infarction with the use of meloxicam was lower than with diclofenac: 0.
09% for a dose of 7.5 mg / day, 0.19% for 15 mg/day and 0.22% for diclofenac 100-150 mg/day.
It should be noted that according to the results of the above work by P. McGettigan and D. Henry [12], meloxicam showed a mild (not exceeding the average level for all NSAIDs), inherent in the entire class of NSAIDs, the ability to increase the risk of developing MI – by about 20% (OR 1.2). According to these data, meloxicam is inferior to naproxen, but is at the level of celecoxib and ibuprofen and superior to diclofenac (OR 1.4, i.e. 40% increased risk).
Comparable results presented by Finnish scientists A. Helin-Salmivaara et al. [36]. They conducted a large population-based study in which the RR of developing NSAID-related CV events was assessed in 33,309 patients with MI (138,949 – corresponding control; Fig. 2 ). data from a population study conducted in Finland: 33,309 patients with MI, 138,949 – controls) [36]. The risk level for those taking meloxicam was at the average level – OR 1.
25. This is somewhat higher than in those taking naproxen (OR 1.19), but clearly less compared to diclofenac (OR 1.35) and especially nimesulide (OR 1.69).
There is a very curious fact: meloxicam was once studied as a component of IHD therapy (!). During the NUT-2 study, 60 patients with acute coronary syndrome who received aspirin and heparin as antithrombotic therapy for 1 month were additionally prescribed meloxicam 15 mg/day. Another 60 patients who underwent similar antithrombotic therapy constituted the control – they were assigned a placebo. Treatment outcomes in the meloxicam group were clearly better. So, among the patients who received this drug, no one developed MI and no patient died; at the same time, there were 2 cases of MI and one coronary death in the control group. In the 1st group, revascularization was required in 6 (10%) patients, and in the 2nd – 15 (25%; р <0.05) [37].
Nowadays, such a study seems rather like medical casuistry; nevertheless, it can serve as a good illustration of the favorable tolerability of meloxicam in patients with risk factors for CVD.
Meloxicam has another important advantage: unlike “traditional” NSAIDs, it does not interact adversely with low doses of aspirin and does not reduce the antiplatelet potential of the latter. This was confirmed by an epidemiological study by G. Singh et al. [38], based on the analysis of the California Database of Patients with MI ( n =15 343). In patients treated with meloxicam in combination with aspirin, the risk of MI was significantly lower than in patients who received this drug without aspirin: OR 0.53 and 1.56, respectively. At the same time, the popular analgesic ibuprofen clearly worsened the effect of aspirin. In patients treated with these drugs together, the risk of MI was even slightly higher than in patients who took ibuprofen alone: OR 1.2 and 1.08, respectively [38].
When discussing the benefits of meloxicam, attention should be paid to the low risk of allergic skin reactions. Although these complications are rare with the use of NSAIDs, in some cases they can be a serious problem.
Meloxicam in this regard is quite safe. Thus, according to American authors, during the first 2 years of using this drug in the United States, not a single episode of Stevens-Johnson syndrome or toxic epidermal necrolysis was recorded (for example, 47 episodes while taking celecoxib) [39]. The low frequency of skin reactions when using meloxicam was also noted by K. Ward et al. [40], who published a methodological review in 2010.
Moreover, there are a number of studies that have shown the possibility of using meloxicam in patients who have previously experienced skin allergic or bronchospastic reactions when using aspirin or other “traditional” NSAIDs [41, 42].
Severe hepatotoxic reactions are also rare side effects of NSAIDs. Nevertheless, the assessment of the risk of complications in the form of liver dysfunction is relevant for a number of representatives of this drug group, such as diclofenac and nimesulide [3]. For example, among 17,289of participants in an 18-month MEDAL RCT (comparison of etoricoxib and diclofenac) who received diclofenac, a three-fold increase in alanine aminotransferase activity was noted in 3.
1%, and a ten-fold increase in 0.5% [43]. Although not a single episode of liver failure or jaundice was recorded, such a clear negative dynamics of biochemical parameters is of concern and is the reason for interrupting therapy.
Fortunately, these problems are not typical for meloxicam.
In the available literature, against the background of treatment with this drug, only isolated cases of asymptomatic, but a significant increase in the level of transaminases or clinically pronounced liver dysfunctions were not noted [44, 45].
Comparative hepatotoxicity of various NSAIDs was studied by Italian authors G. Traversa et al. [46]. They compared the incidence of liver dysfunction in 397,537 patients treated with NSAIDs in 1997-2001. According to the data obtained, meloxicam showed the best tolerance. The frequency of hepatotoxic reactions during its use was 23.6 episodes per 100,000 person-years. A similar indicator for nimesulide, diclofenac and ibuprofen was significant – 35.
2, 39,2 and 44 episodes per 100,000 person-years [46].
Concluding the review, it should be noted that the benefits of any drug are determined not only by successful pharmacological properties and favorable results of clinical trials. For practicing physicians, the “reputation” of the drug is of great importance, which is acquired over the years of its successful use in real clinical practice.
Meloxicam is a representative of NSAIDs, whose good “reputation” is beyond doubt. This drug is well known to doctors all over the world, they trust its effectiveness and good tolerance and actively use it in their work. It should be noted that the good “reputation” of meloxicam is due to a specific original drug, known abroad as mobic (mobic), and in Russia as movalis. It was he who was tested in numerous clinical trials, ultimately proving its therapeutic potential and a favorable tolerability profile. The presence of similar benefits in numerous generic meloxicam still requires strong evidence.
The position of meloxicam (Movalis) among other NSAIDs seems to be the most successful. Of course, this drug cannot be considered completely safe, like any other representative of this drug group. However, it is well tolerated and has a relatively low risk of developing serious complications, in the form of dysfunction of both the gastrointestinal tract and the cardiovascular system; it is quite efficient and easy to use. In general, meloxicam today is the first-line drug for many patients suffering from acute and chronic diseases of the joints and spine.
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Description of the drug Meloxicam is a simplified author’s version of the a.com.ua website.
DO NOT SELF-MEDIATE! IT CAN BE DANGEROUS TO YOUR HEALTH!
Meloxicam: brief instructions for use
Meloxicam is a drug belonging to the group of non-steroidal anti-inflammatory drugs that have analgesic and antipyretic effects.
The composition of Meloxicam includes the main active ingredient – meloxicam. In addition, each tablet contains excipients such as lactose, starch, magnesium and povidone.
Buy Meloxicam is recommended by many experts, as the drug in question shows high anti-inflammatory activity in all models of inflammatory processes without exception.
Indications for use Meloxicam
- Arthritis of rheumatoid type.
- Osteoporosis, osteoarthritis.
- Inflammation localized in the joints.
- Other inflammatory processes accompanied by intense pain.
What are the contraindications to Meloxicam?
- Hypersensitivity to meloxicam or any of the other ingredients of the medicinal product.
- Meloxicam is not recommended for patients who have a history of pathologies such as bronchial asthma, urticaria while taking aspirin and angioedema.
- Pregnancy, lactation and adolescence in patients under 16 years of age.
- Abdominal bleeding that occurred while taking non-steroidal anti-inflammatory drugs.
- Ulcerative lesions of the walls of the gastrointestinal tract.
- Liver or kidney failure.
- Heart or vascular insufficiency.
Interactions of Meloxicam with other drugs
If it is recommended to buy Meloxicam for co-administration with other non-steroidal anti-inflammatory drugs, it should be understood that such drug interactions may significantly increase the risk of bleeding.
Meloxicam significantly enhances the effect of anticoagulants, which can cause bleeding.
At the same time taking this drug with diuretics, there may be a violation of the functioning of the renal system.
Antihypertensive drugs slightly lose their effectiveness when combined with meloxicam components.
Meloxicam: method of administration and dosage
How to take Meloxicam, you can consult your doctor or read the instructions for this drug yourself. The daily dose of the drug is taken once a day during a meal, drinking plenty of water.
In order to minimize the possibility of adverse reactions, the lowest effective dosage is recommended initially. In addition, the specialist must keep the patient’s condition under control, timely conducting all the necessary studies, analyzes and examinations.
Meloxicam should be used with caution in elderly patients. This is justified by the fact that in this age group the risk of negative reactions is significantly increased.
If any side effects are detected, you should immediately inform your doctor about this and stop taking the medication.
Meloxicam is not recommended for patients under 16 years of age.
In the online pharmacy apteka.com, you can check the price of Meloxicam online, as well as place an order for medicines remotely. We will help you decide on the choice of the drug, as well as send the purchase to your address.
Manual Meloxicam
Manufacturer
HELP S.A., Greece
Country of origin
Greece
Synonyms
MELOXICAM, APO-MELOXICAM, AROXICAM, ARTROZAN, ASPIKAM, BI-KSIKAM, ZELOXIM, ZELOXIM FORTE, LOXIDOL, M-KAM®, MELBEK®, MELOX, MELOXAM, MELOXAN, MELOXIC, MELOXICAM, MELOXICAM ORION, MELOKSIKAM PFAYZER ®, MELOXICAM SOPHARMA, MELOXICAM-APO, MELOXICAM-ASTRAPHARM, MELOXICAM-ZENTIVA, MELOXICAM-KV, MELOXICAM-LUGAL, MELOXICAM-MAXPHARMA, MELOXICAM-RATIOPHARM, MELOMAX, MELOMAX™, MOBIK, MOVALGIN, MOVALIS, MOVALIS®, MOVIX,MOVIKSIKAM ®, REVMALGIN, REVMOKSIKAM, REVMOKSIKAM®, RECOX, SANALIS, EXISTEN-SANOVEL
Meloxicam price in online pharmacy ampoule 1.
