mobic and Chronic-Disease

Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used in infants, children, and adolescents worldwide; however, despite sufficient evidence of the beneficial effects of NSAIDs in children and adolescents, there is a lack of comprehensive data in infants. The present review summarizes the current knowledge on the safety and efficacy of various NSAIDs used in infants for which data are available, and includes ibuprofen, dexibuprofen, ketoprofen, flurbiprofen, naproxen, diclofenac, ketorolac, indomethacin, niflumic acid, meloxicam, celecoxib, parecoxib, rofecoxib, acetylsalicylic acid, and nimesulide. The efficacy of NSAIDs has been documented for a variety of conditions, such as fever and pain. NSAIDs are also the main pillars of anti-inflammatory treatment, such as in pediatric inflammatory rheumatic diseases. Limited data are available on the safety of most NSAIDs in infants. Adverse drug reactions may be renal, gastrointestinal, hematological, or immunologic. Since NSAIDs are among the most frequently used drugs in the pediatric population, safety and efficacy studies can be performed as part of normal clinical routine, even in young infants. Available data sources, such as (electronic) medical records, should be used for safety and efficacy analyses. On a larger scale, existing data sources, e.g. adverse drug reaction programs/networks, spontaneous national reporting systems, and electronic medical records should be assessed with child-specific methods in order to detect safety signals pertinent to certain pediatric age groups or disease entities. To improve the safety of NSAIDs in infants, treatment needs to be initiated with the lowest age-appropriate or weight-based dose. Duration of treatment and amount of drug used should be regularly evaluated and maximum dose limits and other recommendations by the manufacturer or expert committees should be followed. Treatment for non-chronic conditions such as fever and acute (postoperative) pain should be kept as short as possible. Patients with chronic conditions should be regularly monitored for possible adverse effects of NSAIDs.

Topics: Adolescent; Anti-Inflammatory Agents; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Celecoxib; Child; Chronic Disease; Diclofenac; Flurbiprofen; Humans; Ibuprofen; Infant; Ketoprofen; Ketorolac; Meloxicam; Naproxen; Niflumic Acid; Pain

Pain is a common feature of childhood and adolescence around the world, and for many young people, that pain is chronic. The World Health Organization guidelines for pharmacological treatments for children's persisting pain acknowledge that pain in children is a major public health concern of high significance in most parts of the world. While in the past pain was largely dismissed and was frequently left untreated, views on children's pain have changed over time, and relief of pain is now seen as important.We designed a suite of seven reviews on chronic non-cancer pain and cancer pain (looking at antidepressants, antiepileptic drugs, non-steroidal anti-inflammatory drugs, opioids, and paracetamol) in order to review the evidence for children's pain utilising pharmacological interventions.As the leading cause of morbidity in the world today, chronic disease (and its associated pain) is a major health concern. Chronic pain (that is pain lasting three months or longer) can arise in the paediatric population in a variety of pathophysiological classifications (nociceptive, neuropathic, or idiopathic) from genetic conditions, nerve damage pain, chronic musculoskeletal pain, and chronic abdominal pain, as well as for other unknown reasons.Non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat pain, reduce fever, and for their anti-inflammation properties. They are commonly used within paediatric pain management. Non-steroidal anti-inflammatory drugs are currently licensed for use in Western countries, however they are not approved for infants under three months old. The main adverse effects include renal impairment and gastrointestinal issues. Common side effects in children include diarrhoea, headache, nausea, constipation, rash, dizziness, and abdominal pain.. To assess the analgesic efficacy and adverse events of NSAIDs used to treat chronic non-cancer pain in children and adolescents aged between birth and 17 years, in any setting.. We searched the Cochrane Central Register of Controlled Trials (CENTRAL) via the Cochrane Register of Studies Online, MEDLINE via Ovid, and Embase via Ovid from inception to 6 September 2016. We also searched the reference lists of retrieved studies and reviews, as well as online clinical trial registries.. Randomised controlled trials, with or without blinding, of any dose and any route, treating chronic non-cancer pain in children and adolescents, comparing any NSAID with placebo or an active comparator.. Two review authors independently assessed studies for eligibility. We planned to use dichotomous data to calculate risk ratio and number needed to treat for one additional event, using standard methods. We assessed GRADE and created three 'Summary of findings' tables.. We included seven studies with a total of 1074 participants (aged 2 to 18 years) with chronic juvenile polyarthritis or chronic juvenile rheumatoid arthritis. All seven studies compared an NSAID with an active comparator. None of the studies were placebo controlled. No two studies investigated the same type of NSAID compared with another. We were unable to perform a meta-analysis.Risk of bias varied. For randomisation and allocation concealment, one study was low risk and six studies were unclear risk. For blinding of participants and personnel, three studies were low risk and four studies were unclear to high risk. For blinding of outcome assessors, all studies were unclear risk. For attrition, four studies were low risk and three studies were unclear risk. For selective reporting, four studies were low risk, two studies were unclear risk, and one study was high risk. For size, three studies were unclear risk and four studies were high risk. For other potential sources of bias, seven studies were low risk. Primary outcomesThree studies reported participant-reported pain relief of 30% or greater, showing no statistically significant difference in pain scores between meloxicam and naproxen, celecoxib and naproxen, or rofecoxib and naproxen (P > 0.05) (low-quality evidence).One study reported participant-reported pain relief of 50% or greater, showing no statistically significant difference in pain scores between low-dose meloxicam (0.125 mg/kg) and high-dose meloxicam (0.25 mg/kg) when compared to naproxen 10 mg/kg (P > 0.05) (low-quality evidence).One study reported Patient Global Impression of Change, showing 'very much improved' in 85% of ibuprofen and 90% of aspirin participants (low-quality evidence). Secondary outcomesAll seven studies reported adverse events. Participants reporting an adverse event (one or more per person) by drug were: aspirin 85/202; fenoprofen 28/49; ibuprofen 40/45; indomethacin 9/30; ketoprofen 9/30; meloxicam 18/47; naproxen 44/202; and rofecoxib 47/209 (very low-quality evidence).All seven studies reported withdrawals due to adverse events. Participants withdrawn due to an adverse event by drug were: aspirin 16/120; celecoxib 10/159; fenoprofen 0/49; ibuprofen 0/45; indomethacin 0/30; ketoprofen 0/30; meloxicam 10/147; naproxen 17/285; and rofecoxib 3/209 (very low-quality evidence).All seven studies reported serious adverse events. Participants experiencing a serious adverse event by drug were: aspirin 13/120; celecoxib 5/15. We identified only a small number of studies, with insufficient data for analysis.As we could undertake no meta-analysis, we are unable to comment about efficacy or harm from the use of NSAIDs to treat chronic non-cancer pain in children and adolescents. Similarly, we cannot comment on our remaining secondary outcomes: Carer Global Impression of Change; requirement for rescue analgesia; sleep duration and quality; acceptability of treatment; physical functioning; and quality of life.We know from adult randomised controlled trials that some NSAIDs, such as ibuprofen, naproxen, and aspirin, can be effective in certain chronic pain conditions.

Topics: Adolescent; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Juvenile; Arthritis, Rheumatoid; Aspirin; Celecoxib; Child; Child, Preschool; Chronic Disease; Chronic Pain; Fenoprofen; Humans; Ibuprofen; Lactones; Meloxicam; Methoxsalen; Naproxen; Randomized Controlled Trials as Topic; Sulfones; Thiazines; Thiazoles

The purpose of this study was to define the role of cyclooxygenase-2 inhibitors (COX-2i) in reducing hepatic fibrosis in pediatric patients with chronic liver disease.. From September 2009 to September 2010, patients over 2 years old who visited our outpatient clinic for follow-up to manage their chronic liver disease after Kasai portoenterostomy for biliary atresia, were included in this study. Volunteers were assigned to the study or control groups, according to their preference. A COX-2i was given to only the study group after obtaining consent. The degree of hepatic fibrosis (liver stiffness score, LSS) was prospectively measured using FibroScan, and liver function was examined using serum analysis before and after treatment. After 1 year, changes in LSSs and liver function were compared between the two groups.. Twenty-five patients (18 females and 7 males) were enrolled in the study group. The control group included 44 patients (26 females and 18 males). After 1 year, the least square mean values for the LSSs were significantly decreased by 3.91±0.98 kPa (p=0.004) only in the study group. Serum total bilirubin did not decrease significantly in either group.. COX-2i treatment improved the LSS in patients with chronic liver disease after Kasai portoenterostomy for biliary atresia.

Topics: Biliary Atresia; Child; Child, Preschool; Chronic Disease; Cyclooxygenase 2 Inhibitors; Female; Humans; Liver Cirrhosis; Male; Meloxicam; Portoenterostomy, Hepatic; Thiazines; Thiazoles

To evaluate the effects of adjunctive meloxicam administration on clinical periodontal measurements and gingival crevicular fluid (GCF) prostaglandin E(2) (PGE(2)) and interleukin-1-beta (IL-1beta) levels in chronic periodontitis.. Forty chronic periodontitis patients were randomized to receive either meloxicam 7.5 mg or placebo tablets for 10 days with scaling and root planing (SRP). GCF levels of PGE(2) and IL-1beta at baseline, day 10 of drug intake and 4 weeks after SRP were determined by enzyme-linked immunosorbent assay. Demographic, clinical periodontal data were analyzed using a repeated measures ANOVA and Bonferroni analysis. GCF PGE(2) and IL-1beta levels were compared between different evaluation times using the Friedman test. The Mann-Whitney test was used to compare biochemical data between the study groups. Pearson correlation analysis was used to relate clinical and biochemical data.. Study groups showed significant reductions in all clinical periodontal measurements and GCF volume (p < 0.05). In both groups, IL-1beta was reduced significantly on day 10 and at week 4 compared with baseline (p < 0.01) without significant changes in PGE(2) levels (p > 0.05). No significant differences were found between study groups in GCF IL-1beta or PGE(2) levels (p > 0.05).. Adjunctive meloxicam does not seem to provide additional improvement in clinical parameters or GCF PGE(2) and IL-1beta levels. Larger-scale studies may better clarify potential usage of anti-inflammatory agents in periodontal therapy.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Chronic Disease; Dinoprostone; Double-Blind Method; Female; Gingival Crevicular Fluid; Humans; Interleukin-1beta; Male; Meloxicam; Middle Aged; Periodontitis; Placebos; Thiazines; Thiazoles

The aim of the present study was to determine the effects of meloxicam after initial periodontal treatment on interleukin-1beta (IL-1beta) and IL-1 receptor antagonist (IL-1ra) in gingival crevicular fluid (GCF) and clinical parameters in the chronic periodontitis patients. Data were obtained from 30 patients with chronic periodontitis. Fifteen chronic periodontitis patients received 7.5 mg meloxicam, and 15 patients received placebo tablets in a 1x1 regimen for 1 month. All subjects were nonsmokers and had not received any periodontal therapy. The plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) were recorded. The GCF was collected using a paper strip: eluted and enzyme-linked immunoabsorbent assays (ELISAs) were performed to determine the cytokine levels. The clinical data and GCF samples were obtained after periodontal therapy and 1 month after periodontal therapy. The PI, GI, PD, and GCF IL-1ra decreased significantly (p<0.05) in meloxicam group at first month when comparing the initial levels. While decrease of the PI was statistically significant in control group (p<0.05), statistically significant changes were not determined in the other clinical parameters and GCF cytokine levels (p>0.05). There were no significant differences between two groups in any of the investigated parameters. Our observations did not reveal any influence of meloxicam on levels of IL-1beta and IL-1ra in chronic periodontitis. Additional clinical studies are advisable to determine whether COX-2 selective drugs alter periodontal disease outcome with greater safety.

Topics: Adult; Chronic Disease; Cyclooxygenase Inhibitors; Epidemiologic Methods; Female; Gingival Crevicular Fluid; Humans; Interleukin 1 Receptor Antagonist Protein; Interleukin-1beta; Male; Meloxicam; Middle Aged; Periodontitis; Thiazines; Thiazoles

The efficacy, tolerance and ease of administration of a nutraceutical, carprofen or meloxicam were evaluated in a prospective, double-blind study on 71 dogs with osteoarthritis. The client-owned dogs were randomly assigned to one of the three treatments or to a placebo control group. The influence of osteoarthritis on the dogs' gait was described by comparing the ground reaction forces of the arthritic dogs and 10 normal dogs. Before the treatments began, and 30 and 60 days later, measurements were made of haematological and biochemical variables and of the ground reaction forces of the arthritic limb, and subjective assessments were made by the owners and by the orthopaedic surgeons. Changes in the ground reaction forces were specific to the arthritic joint, and were significantly improved by carprofen and meloxicam but not by the nutraceutical; the values returned to normal only with meloxicam. The orthopaedic surgeons assessed that there had been an improvement with carprofen and meloxicam, but the owners considered that there had been an improvement only with meloxicam. The blood and faecal analyses did not reveal any changes. The treatments were well tolerated, except for a case of hepatopathy in a dog treated with carprofen.

Topics: Administration, Oral; Animals; Anti-Inflammatory Agents, Non-Steroidal; Ascorbic Acid; Carbazoles; Chondroitin Sulfates; Chronic Disease; Dog Diseases; Dogs; Double-Blind Method; Gait; Glucosamine; Lameness, Animal; Manganese Compounds; Meloxicam; Osteoarthritis; Osteoarthritis, Hip; Osteoarthritis, Knee; Prospective Studies; Severity of Illness Index; Stifle; Thiazines; Thiazoles; Treatment Outcome

The purpose of the present study was to assess the effects of adjunctive meloxicam on the matrix metalloproteinase-8 (MMP-8) levels of gingival crevicular fluid (GCF) in chronic periodontitis patients following the initial phase of periodontal therapy.. Twelve chronic periodontitis patients received 7.5 mg meloxicam, and 10 patients received placebo tablets together with scaling and root planing in a 1 x 1 regimen for 10 days. Scaling and root planing were performed on day 3 of drug intake. The MMP-8 levels in GCF samples obtained before and on day 10 of drug intake were determined by using the immunofluorescence assay. Plaque index (PI), papilla bleeding index (PBI), and GCF MMP-8 levels were compared within each patient group, between the 2 patient groups, and also with a clinically healthy control group using non-parametric statistical analyses.. Both meloxicam and placebo groups showed statistically significant reductions in PBI, PI, and GCF MMP-8 levels on day 10 compared to baseline (P<0.01). The GCF MMP-8 level on day 10 in the meloxicam group was similar to the clinically healthy control group (P>0.05), while it was significantly higher in the placebo group (P<0.01). Positive correlations were found between MMP-8 total amounts and PBI scores at baseline and day 10 of drug intake in the patient groups.. Meloxicam showed a tendency to reduce GCF MMP-8 levels in vivo within the first 10 days when used as an adjunct in the initial phase of periodontal treatment that consists of scaling and root planing. Verification of this effect on collagenase-2 downregulation, as well as on the clinical periodontal parameters in long-term studies using larger test and control groups, is needed to provide further support for the adjunctive use of selective cyclooxygenase (COX)-2 inhibitors in the treatment of chronic periodontitis.

Topics: Adult; Alveolar Bone Loss; Chronic Disease; Combined Modality Therapy; Cyclooxygenase Inhibitors; Dental Plaque Index; Dental Scaling; Double-Blind Method; Female; Fluorescent Antibody Technique; Follow-Up Studies; Gingival Crevicular Fluid; Humans; Isoenzymes; Male; Matched-Pair Analysis; Matrix Metalloproteinase 8; Meloxicam; Middle Aged; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Periodontitis; Placebos; Root Planing; Statistics, Nonparametric; Thiazines; Thiazoles

In this randomised, multicentre clinical study, dogs with musculoskeletal pain and inflammation were treated with either vedaprofen or meloxicam administered orally at the recommended dose rates. Clinical examinations were carried out regularly and clinical severity scores assigned. In total, 214 cases (73 acute, 141 chronic) were evaluated. Treatment with vedaprofen and meloxicam was continued for 14 and 17 days, respectively, in the acute cases, and 38 and 39 days in the chronic cases. NSAID treatment resulted in a significant improvement in clinical scores. The overall response to treatment ('responders') at the final clinical examination was 89 per cent and 87 per cent in the acute cases and 72 per cent and 65 per cent in the chronic cases in the vedaprofen and meloxicam groups, respectively. Mild transient gastrointestinal signs were observed in both groups (11 per cent vedaprofen, 12 per cent meloxicam). Adverse effects related to NSAIDs resulted in treatment cessation in 5 per cent of the dogs in each group. Vedaprofen and meloxicam were efficacious in, and well tolerated by, most of the dogs in the study.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents, Non-Steroidal; Chronic Disease; Dog Diseases; Dogs; Female; Inflammation; Male; Meloxicam; Musculoskeletal Diseases; Naphthalenes; Pain; Propionates; Thiazines; Thiazoles; Treatment Outcome

A clinical trial was conducted to evaluate the safety and efficacy of the nonsteroidal anti-inflammatory drug meloxicam in dogs with chronic osteoarthritis. Forty clinical cases were enrolled in the 2-phase study. Phase 1 compared therapeutic efficacy and tolerance of meloxicam or placebo for 1 week. Phase 2 involved a 4-week evaluation of the drug's clinical efficacy and tolerance. Clinical efficacy was evaluated by using a scoring system that assessed specific lameness, general stiffness, painful rise, exercise intolerance, and behavior. Evaluations demonstrated significant reductions (P < 0.05) in clinical signs of osteoarthritis following 4 weeks of drug therapy. Side effects were minimal in extent and duration. The drug was accepted without problems in the majority of cases. The findings of this investigation suggest that the efficacy, tolerance, and formulation of meloxicam oral suspension make it well suited for the treatment of chronic osteoarthritis in the dog.

Topics: Administration, Oral; Animals; Anti-Inflammatory Agents, Non-Steroidal; Chronic Disease; Dog Diseases; Dogs; Female; Male; Meloxicam; Osteoarthritis; Thiazines; Thiazoles; Treatment Outcome

122 patients with osteoarthrosis, who have in the past medical history verified chronic gastritis (50 males and 72 females) at the age from 42 to 64 have been examined. Control group was comprised of 40 patients with osteoarthrosis without gastroduodenal zone pathology in the past medical history. For arthralgia relief patients were prescribed meloxicam (average dose--12.5 - 1.39 mg daily) or nimesulide (average dose--150 ± 14.91 mg daily). As a result of this research it was determined that administration of selective NSAID (meloxicam and nimesulide) in patients with chronic gastritis in the past medical history raised the risk of NSAID gastropathy/dyspepsia 2.9 times (P < 0.03) than in patients without associated gastroduodenal zone pathology. Atrophy of gastric mucosa is associated with higher risks (P > 0.05) of erosive gastropathy. Patients with chronic gastritis in the past medical history when taking NSAID with the purpose of gastropathy prevention are recommended to undergo gastroprotective therapy.

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Chronic Disease; Female; Gastritis; Humans; Male; Meloxicam; Middle Aged; Osteoarthritis; Protective Agents; Sulfonamides; Thiazines; Thiazoles

Topics: Adult; Arthralgia; Arthritis; Chronic Disease; Coagulants; Cyclooxygenase Inhibitors; Exercise Therapy; Factor IX; Factor VIII; Hemophilia A; Humans; Meloxicam; New Zealand; Patient Satisfaction; Thiazines; Thiazoles

Cyclooxygenase isoenzyme is known to be expressed in different regions of brain, and is mainly used for the treatment of pain and inflammation. Recently, it is proposed that cyclooxygenase isoenzyme may also play a key role in the pathophysiology of various brain-related disorders. The present study was aimed to explore the protective effect of cyclooxygenase inhibitors on stress by using an animal model of chronic stress.. The animals were forced to swim individually for a period of 6 min every day for 15 d. Then, the behavior (locomotor activity, anxiety and memory) and biochemical (lipid peroxidation, nitrite level, reduced glutathione, and catalase) alterations were assessed.. Forced swimming for 15 d caused impaired locomotor activity, anxiety-like behavior and decreased percentage of memory retention, as compared to naive mice (without chronic fatigue treatment). Biochemical analysis revealed significant increases in lipid peroxidation and nitrite level, while levels of reduced glutathione and catalase activity were both decreased. Chronic treatment with naproxen (14 mg/kg, i.p.), rofecoxib (5 mg/kg, i.p.), meloxicam (5 mg/kg, i.p.), nimesulide (5 mg/kg, i.p.) and valdecoxib (10 mg/kg, i.p.) significantly attenuated these behavioral and biochemical (oxidative damage) alterations in chronic-stressed mice.. The cyclooxygenase inhibitors could be used in the management of chronic fatigue-like conditions.

Topics: Animals; Anxiety; Catalase; Chronic Disease; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Disease Models, Animal; Glutathione; Isoxazoles; Lactones; Lipid Peroxidation; Male; Meloxicam; Memory; Mice; Motor Activity; Naproxen; Nitrites; Random Allocation; Stress, Psychological; Sulfonamides; Sulfones; Thiazines; Thiazoles

Chronic arthritis leads to a decrease in body weight that is associated with a decrease in skeletal muscle and white adipose tissue mass. We have observed that overactivation of cyclooxygenase-2 (COX-2) is responsible for muscle wasting in arthritic rats. The aim of this work was to study the role of COX-2 in arthritis-induced white adipose tissue mass loss. Arthritis was induced in rats by Freund's adjuvant injection, and the effect of the COX-2 inhibitor meloxicam on serum concentrations of leptin, adiponectin, insulin and glycerol, as well as on gene expression of leptin, adiponectin, hormone-sensitive lipase (HSL), fatty acid synthase (FAS), tumour necrosis factor alpha (TNF) and insulin-like growth factor I (IGF-I) in white adipose tissue were determined. Arthritis decreased adipose tissue weight, serum leptin and adiponectin as well as their mRNAs in adipose tissue. Meloxicam administration to arthritic rats increased adipose tissue weight, serum concentrations of adiponectin and its mRNA in adipose tissue, but it did not modify leptin. Arthritis decreased serum insulin and FAS and IGF-I gene expression in adipose tissue. Meloxicam administration did not modify these effects. Serum concentrations of glycerol were decreased in arthritic rats. In control rats, meloxicam administration did not modify serum glycerol or adipose tissue gene expression of HSL. However, in arthritic rats HSL gene expression in adipose tissue was decreased by meloxicam. All these data indicate that COX-2 activation plays a role in the decrease in adiponectin secreted by adipocytes and in the loss in white adipose tissue mass in arthritic rats.

Topics: Adiponectin; Adipose Tissue, White; Animals; Arthritis, Experimental; Body Weight; Chronic Disease; Cyclooxygenase 2; Cyclooxygenase Inhibitors; Insulin-Like Growth Factor I; Male; Meloxicam; Rats; Rats, Wistar; RNA, Messenger; Severity of Illness Index; Thiazines; Thiazoles; Tumor Necrosis Factor-alpha

Meloxicam is a non-steroidal anti-inflammatory drug (NSAID) that primarily has an antiproteinuric effect and is used for the treatment of chronic glomerular diseases. In chronic glomerular disease (CGD), proteinuria is involved in the production of tubulo-interstitial lesions and has an important role in their progression. CGD improves with steroid therapy and immunosuppression. In the case of a favorable outcome, a reduction in proteinuria is also attained. In some situations, this therapy is prohibited, requiring alternative medication. NSAIDs are one class of these alternative drugs; in addition to having anti-inflammatory actions, they also have antiproteinuric effects. The aim of the study has been to assess the effect of the anti-inflammatory treatment with meloxicam upon proteinuria as well as upon tubular lesions by determining urinary NAG in its dynamics. The study was performed on 12 patients with CGD, 6 of them with nephrotic syndrome. On all patients we administered treatment with meloxicam 15 mg/day, 30 days. On all patients we performed proteinuria and urinary N-acetyl b D glucosaminidase (NAG) at the beginning, after 7 days and after 30 days of treatment. A 24-hour urine collection was taken from all patients. The urinary protein concentration was determined with the use of the Dimension (Dade Behring, Inc., Newark, DE, USA) clinical chemistry system UCFP method. We found a decrease of proteinuria under treatment from 2.85 +/- 1.69 g/24h to 1.53 +/- 0.83 g/24h, which was significantly lower, compared to the initial measurement (p = 0.01878). After 30 days of treatment with meloxicam, urinary NAG decreased from 10.6 +/- 12.56 U/g creatinine to 6.44 +/- 7 U/g, a decrease that was statistically non-significant. We observed a strong correlation between initial urinary NAG and initial proteinuria ri = 0.924, p < 0.001 and between final urinary NAG and final proteinuria rf = 0.856, p < 0.001. Our study revealed the favorable effect of meloxicam on patients with CGD on a 30-day treatment phase reflected on the evolution of proteinuria. Only in one case we did reveal a possible deleterious effect of this treatment. The assessment of the effect on tubulo-interstitial lesions in this short treatment period through urinary NAG assessment indicated only a modest and statistically non-significant response. We consider that meloxicam can be a useful drug in the treatment of proteinuric glomerular diseases.

Topics: Acetylglucosaminidase; Adult; Anti-Inflammatory Agents, Non-Steroidal; Chronic Disease; Female; Glomerular Filtration Rate; Glomerulonephritis; Humans; Male; Meloxicam; Proteinuria; Thiazines; Thiazoles

This study describes the use of a simple questionnaire-based tool to identify behavioural/lifestyle changes that are associated with chronic pain in the cat. These changes were grouped into four behavioural domains (mobility, activity, grooming and temperament). Twenty-three cats with chronic musculoskeletal pain as determined by clinical examination were included. The owners of these cats were asked to complete a questionnaire before and 28 days after the start of analgesic treatment (meloxicam). This included a global assessment of changes in behaviour and assessment of the degree of behavioural change observed within each of the defined domains. The attending veterinary surgeon was independently asked to provide a global score before and after treatment. Both owners and veterinary surgeons reported significant changes in behaviour/lifestyle after analgesic therapy. There was no difference between the owners and veterinary surgeons global assessments at baseline but there was at day 28 (P=0.02). The owners' scores decreased from a median of 5 at baseline to 3 at 28 days (P=0.0004) while the median veterinary surgeon scores decreased from 5 to 2 at 28 days (P<0.0001). There was a statistically significant reduction in the owners' scores for each of the four domains with the greatest reduction occurring in the activity category (P=0.0001). This study shows that owner assessment of changes in their cat's behaviour/lifestyle is an important method of identifying chronic pain in their pets.

Topics: Analgesics; Animals; Behavior, Animal; Cat Diseases; Cats; Chronic Disease; Dogs; Female; Human-Animal Bond; Male; Meloxicam; Musculoskeletal Diseases; Pain; Pain Measurement; Severity of Illness Index; Thiazines; Thiazoles; Time Factors; Treatment Outcome

Chronic arthritis induces cachexia associated with an inhibition of the growth hormone (GH)-insulin-like growth factor-I (IGF-I) system and an activation of the E3 ubiquitin-ligating enzymes muscle atrophy F-box (MAFbx) and muscle Ring finger 1 (MuRF1) in the skeletal muscle. The aim of this work was to study the role of cyclooxygenase (COX)-2 in chronic arthritis-induced cachexia. Arthritis was induced in rats by Freund's adjuvant injection, and the effects of two COX inhibitors (indomethacin, a nonspecific inhibitor, and meloxicam, a selective COX-2 inhibitor on pituitary GH and on liver and serum IGF-I levels) were tested. Arthritis decreased body weight gain and GH and liver IGF-I gene expression. In the arthritic rats, both inhibitors, indomethacin and meloxicam, prevented the inhibitory effect of arthritis on body weight gain. Indomethacin and meloxicam administration to arthritic rats increased pituitary GH and liver IGF-I mRNA as well as serum levels of IGF-I. These data suggest that induction of COX-2 during chronic inflammation is involved in the inhibition of the GH-IGF-I axis and in the body weight loss. In the gastrocnemius muscle, arthritis increased the gene expression of tumor necrosis factor (TNF)-alpha, the E3 ubiquitin-ligating enzymes MAFbx and MuRF1, as well as of IGF-I and IGF-binding protein-5 (IGFBP-5). Inhibition of COX-2 by meloxicam administration increased gastrocnemius weight and decreased MAFbx, MuRF1, TNF-alpha, and IGFBP-5 gene expression. In summary, our data indicate that chronic arthritis-induced cachexia and muscle wasting are mediated by the COX-2 pathway resulting in a decreased GH-IGF-I secretion and increased expression of MAFbx and MuRF1 mRNA.

Topics: Animals; Arthritis, Experimental; Cachexia; Chronic Disease; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Enzyme Activation; Gene Expression; Growth Hormone; Indomethacin; Insulin-Like Growth Factor Binding Protein 5; Insulin-Like Growth Factor I; Liver; Male; Meloxicam; Muscle Proteins; Muscle, Skeletal; Pituitary Gland; Rats; Rats, Wistar; RNA, Messenger; SKP Cullin F-Box Protein Ligases; Thiazines; Thiazoles; Tripartite Motif Proteins; Tumor Necrosis Factor-alpha; Ubiquitin-Protein Ligases; Weight Gain

Fecal alpha(1)-proteinase inhibitor (alpha(1)-PI) clearance is a reliable, noninvasive marker for protein-losing enteropathy (PLE) in human beings. An assay for measurement of this protein in the dog has been developed and validated and may be useful for the investigation of gastrointestinal disease in this species. Nonsteroidal anti-inflammatory drugs (NSAIDs) frequently are administered to dogs and may have adverse effects on the gastrointestinal tract, including gastroduodenal ulceration and altered mucosal permeability. The value of fecal alpha(1)-PI measurement in detecting unrelated gastrointestinal disease may be limited in dogs on NSAID therapy, but alpha(1)-PI may be a useful marker for NSAID-induced gastrointestinal damage.. The aim of this study was to evaluate the effects of long-term administration of NSAIDs on fecal alpha(1)-PI concentrations in dogs.. Fecal samples were collected from 2 groups of dogs: 1) 21 clinically-healthy client-owned dogs without signs of gastrointestinal disease and receiving no NSAIDs and 2) 7 dogs referred for investigation and treatment of orthopedic disorders; the dogs had received either meloxicam or carprofen daily for at least 30 days. Fecal alpha(1)-PI concentration was measured by ELISA.. Fecal alpha(1)-PI concentrations, expressed as micro g/g of feces, were not significantly different between groups 1 and 2 (median [range], group 1: 9.9 micro g/g [0.0-32.1 micro g/g]; group 2: 5.6 micro g/g [1.1-32.3 micro g/g]; P =.81).. These results suggest that use of cyclooxygenase-2-selective NSAIDs, such as carprofen and meloxicam, does not significantly affect fecal alpha(1)-PI measurements. However, study numbers were small, and larger prospective trials are required to assess more accurately the gastrointestinal effects of NSAIDs in dogs.

Topics: alpha 1-Antitrypsin; Animals; Anti-Inflammatory Agents, Non-Steroidal; Carbazoles; Case-Control Studies; Chronic Disease; Dog Diseases; Dogs; Enzyme-Linked Immunosorbent Assay; Feces; Female; Male; Meloxicam; Protein-Losing Enteropathies; Thiazines; Thiazoles

Prostaglandins (PG) derived from COX-1 are essential for the maintenance of mucosal integrity but COX-2 isoform synthesizes PG at a site of inflammation. Recently, COX-2 mRNA expression was demonstrated at the ulcer edge during healing of chronic gastric ulcers but the role for expression of COX-2 and its products such as PGE(2) and cytokines including interleukin (IL-1beta) and tumor necrosis factor alpha (TNFalpha) in ulcer healing remains unknown. In this study, Wistar rats with gastric ulcers produced by serosal application of acetic acid (ulcer area 28 mm(2)) received daily treatment either with: (1) vehicle (saline); (2) NS-398 (10 mg/kg-d i.g.) and Vioxx (5 mg/kg-d i.g.), both, highly specific COX-2 inhibitors; (3) meloxicam (5 mg/kg-d i.g.), a preferential inhibitor of COX-2; (4) resveratrol (10 mg/kg-d i.g.), a specific COX-1 inhibitor; (5) indomethacin (5 mg/kg-d i.g); and (6) aspirin (ASA; 50 mg/kg-d i.g.), non-selective inhibitors of both COX-1 and COX-2. At day 3, 7, and 14 after ulcer induction, the animals were sacrificed and the area of gastric ulcers was determined by planimetry and histology, gastric blood flow (GBF) at ulcer base and margin was measured by H(2) clearance technique, and blood was withdrawn for measurement of plasma IL-1beta and TNFalpha levels. The mucosal biopsy samples were taken for the determination of PGE(2) generation by RIA and expression of COX-1, COX-2, IL-1beta, and TNFalpha mRNA by RT-PCR. In vehicle-treated rats, gastric ulcers healed progressively and at day 14 the healing was completed, accompanied by a significant rise in the GBF at ulcer margin. The IL-1beta, TNFalpha, and COX-1 mRNA were detected in intact and ulcerated gastric mucosa, whereas COX-2 mRNA were upregulated only in ulcerated mucosa with peak observed at day 3 after ulcer induction. The plasma IL-1beta level was significantly increased at day 3 and 7 but then declined at day 14 to that measured in vehicle-controls. Indomethacin and ASA, which suppressed PGE(2) generation both in the non-ulcerated and ulcerated gastric mucosa, significantly delayed the rate of ulcer healing and this was accompanied by the fall in GBF at ulcer margin and further elevation of plasma IL-1beta and TNFalpha levels, which was sustained up to the end of the study. Treatment with NS-398 and Vioxx, which caused only a moderate decrease in the PGE(2) generation in the non-ulcerated gastric mucosa, delayed ulcer healing and attenuated significantly the GBF at ulcer marg

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Chronic Disease; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprostone; Gastric Mucosa; Gastrins; Indomethacin; Interleukin-1; Isoenzymes; Lactones; Male; Meloxicam; Membrane Proteins; Nitrobenzenes; Prostaglandin-Endoperoxide Synthases; Radioimmunoassay; Rats; Rats, Wistar; Resveratrol; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Stilbenes; Stomach Ulcer; Sulfonamides; Sulfones; Thiazines; Thiazoles; Tumor Necrosis Factor-alpha

Adverse reactions to nonsteroidal anti-inflammatory drugs (NSAIDs) are frequent, particularly among patients with chronic urticaria or asthma. The need to identify an alternative drug that is safe and reliable is a common problem in clinical practice.. To assess the tolerability of meloxicam, a new NSAID that selectively inhibits the inducible isoform of cyclooxygenase, in a group of NSAID-sensitive patients.. We studied 177 patients who had suffered adverse reactions to one or more NSAIDs. Cutaneous reactions were reported by 83.1% of the subjects (urticaria in 55, angioedema in 52, urticaria/angioedema in 39, and maculopapular rash in 1), respiratory symptoms by 3.9%, both cutaneous and respiratory symptoms by 9%, Stevens-Johnson's syndrome by 2.3%, and anaphylactoid reactions by 1.7%. All subjects underwent a single-blind, placebo-controlled oral challenge with divided therapeutic doses of meloxicam (1.9 mg + 5.6 mg 1 hour later = cumulative dose 7.5 mg).. Positive reactions were observed in only two cases (1.1%), both manifested exclusively by cutaneous symptoms (urticaria/angioedema in one case and maculopapular rash/facial edema in the second).. Meloxicam seems to be well tolerated by NSAID-sensitive subjects whose reactions are manifested by urticaria/angioedema. Additional study is needed for a more complete assessment of its tolerability in patients with aspirin-induced asthma and other severe manifestations of NSAID sensitivity.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anaphylaxis; Angioedema; Anti-Inflammatory Agents, Non-Steroidal; Asthma; Chronic Disease; Cyclooxygenase Inhibitors; Drug Eruptions; Female; Forced Expiratory Volume; Humans; Male; Meloxicam; Middle Aged; Thiazines; Thiazoles; Urticaria