Oral Diclofenac Sodium Research Articles

Efficacy of a prolonged-release dosage form of diclofenac sodium in some rheumatic diseases

Twenty outpatients suffering from rheumatoid arthritis and 20 outpatients with scapulohumeral periarthritis were treated for 30 days with oral diclofenac sodium, either using one 150-mg prolonged-release capsule per day (10 patients with each diagnosis) or one 50-mg, enteric-coated tablet 3 times a day (10 patients per diagnosis). During treatment, visual analog scale scores for pain intensity, the severity of symptoms and signs, and results of laboratory tests (erythrocyte sedimentation rate, C-reactive protein, and rheumatoid factor) were monitored, as well as the local tolerability of the administered formulations. Systemic tolerability was also monitored by means of routine blood and urine laboratory tests. The single daily administration of 150 mg as a prolonged-release capsule dosage form yielded almost identical and very good anti-inflammatory and analgesic activity as the multiple daily administration of the 50-mg tablet: 16 cases of good activity and 4 of no efficacy with the prolonged-release formulation versus 15 cases of good efficacy and 5 cases of no efficacy with the enteric-coated tablet. As predictable, based on the different characteristics of the diseases, some patients with rheumatoid arthritis responded only partially to diclofenac treatment (60% had positive results), while in nearly all patients with scapulohumeral periarthritis, treatment with this nonsteroidal anti-inflammatory drug yielded the best clinical outcome (95% had positive results). Drug tolerability, both at the gastrointestinal and systemic levels, was excellent; no adverse events were reported. The prolonged-release formulation, which enables once-daily dosing, appears to be an optimal means to treat articular rheumatic diseases.

The Effect of Diclofenac Sodium on Urinary Concentration of Calcium, Uric Acid and Glycosaminoglycans in Traumatic Paraplegics

Non-steroidal anti-inflammatory drugs (NSAID) have been shown to decrease calcium excretion in the experimental animal, in human volunteers and in calcium stone formers. Paraplegics tend to be hypercalciuric during the first 2 years after their injury and this is said to be a predisposing factor for stone formation in these patients. The effect of the NSAID diclofenac sodium was studied in 12 traumatic paraplegics who had sustained their injury 1 to 6 months previously; 24-h urine samples collected before and 2 weeks and 4 weeks after oral diclofenac sodium 50 mg tds were analysed for calcium, uric acid, glycosaminoglycans (GAGs) and volume. There were no significant changes in urinary volume, uric acid and GAGs excretion. However, urinary calcium concentration and 24-h calcium excretion decreased significantly following 2 weeks' and 4 weeks' treatment with diclofenac sodium.

Comparative bioavailability of diclofenac hydroxyethylpyrrolidine vs diclofenac sodium in man

A phamacokinetic study in man has been made of a new dosage form of diclofenac hydroxyethylpyrrolidine (DIEP); soluble salt packed in sachets was compared with diclofenac sodium as enteric coated tablets. Oral DIEP 2 X 50 mg showed a significant difference in absorption kinetics (ka, lag time and tmax) as compared to oral diclofenac sodium 2 X 50 mg. A relevant plasma concentration of diclofenac was detected just 15 min after DIEP, while diclofenac sodium produced a measurable plasma concentration only 0.5-1 h after the treatment. Cmax and t1/2 after DIEP and diclofenac sodium were comparable. Comparison of the two AUC values showed that DIEP was bioequivalent to diclofenac sodium (Q = 100%).

Double-blind evaluation of analgesic efficacy of orally administered diclofenac, nefopam, and acetylsalicylic acid (ASA) plus codeine in chronic cancer pain

The analgesic efficacy and toxicity of oral diclofenac sodium 50 mg (q.i.d.) vs. nefopam 60 mg (q.i.d.) and a combination of 640 mg ASA and 40 mg codeine (q.i.d.) in cancer patients with moderate to severe chronic pain has been evaluated in a randomized double-blind study. Planned duration of treatment was 10 days. Pain intensity was evaluated by a visual analog scale. The length of patient participation in the trial, the patient's final global evaluation and the incidence of side effects were also evaluated. Ninety-nine patients were enrolled in the study. All treatments produced a statistically significant pain relief ( P < 0.01) without differences among groups but only 26 of 99 patients (26.3%) completed the planned treatment period. Mean time in the study was 4.65 days. Inefficacy and side effects were the main reasons for premature treatment interruption. Patients treated with nefopam had a significantly shorter period in the study than patients treated with the other 2 treatments. Adverse effects were slightly more frequent with the nefopam and ASA + codeine regimens. The 3 therapeutic regimens appear to be similar as to analgesic efficacy, but diclofenac presents the advantage of a slightly better safety profile than nefopam and the ASA + codeine combination.

A study of the effect of aspirin on the pharmacokinetics of oral and intravenous diclofenac sodium.

Previous studies have shown that aspirin interacts with orally administered diclofenac sodium, causing reduced peak concentrations, lower levels and decreased areas under curves. In this study, diclofenac sodium was administered orally and intravenously with and without aspirin, to 6 healthy female volunteers. After intravenous dosing both plasma levels and areas under curves were significantly reduced although none of the rate constants was affected. The volume of distribution of diclofenac was increased as was the plasma clearance. Oral administration with aspirin also resulted in lower plasma levels, particularly peak levels, and areas under curves. Comparison of AUC's for both modes of administration with and without aspirin suggested that lower levels after oral administration were not due to impaired absorption. These observations are best explained by decreased protein binding and increased biliary excretion of diclofenac in the presence of salicylate.