Oligoclonal immunoglobulins and smooth muscle antibodies in arthritic joints.

In twelve synovial fluid/serum pairs from patients with various types of seronegative polyarthritis, homogeneous gamma-bands by agarose gel electrophoresis were found in seven of the synovial fluids and in only one of the sera. In six of the fluids with gamma-bands, smooth muscle antibodies (SMA) were also present, usually in a titre identical to that in serum. In fluids with no gamma-bands, no SMA were detected. In forty synovial fluid/serum pairs from paitients with seropositive rheumatoid arthritis, no gamma-bands were detected in the synovial fluids, and SMA were present in only three pairs. Absorption and inhibition experiments did not give evidence that the SMA activity in seronegative polyarthritis was confined to the gamma-bands in the synovial fluids. The SMA activity in the fluids seemed to be directed against both actin and 'non-actin' muscular antigens. The association between locally produced oligoclonal immunoglobulins and possible locally produced SMA with differnet electrophoretic mobility suggests that in some of thes patients there is a local synovial production of oligoclonal antibodies with different specificities. Thus, even if the results may indicate a local virus infection in some arthritic joints, they may also be dur to an unspecific local stimulation of B cells or to a specific antigen stimulation combined with an unspecific co-activation of other antibody-producing cells.

Polymyalgia arteritica. A report on five cases within a family.

This work describes four patients with polymyalgia arteritica (PMA) and one patient with an illness compatible with PMA within one family. Of these 5 patients, 4 are siblings while one is a genetically unrelated husband. The husband had a classical GCA in 1969. Over a period of one year starting in 1975, the husband's wife and three of her siblings were affected with PMA. This observation is highly suggestive of an infectious agent as being responsible for PMA, and a genetic disposition is probably essential for development of the disease. The incubation period is probably in the range of 5--7 years.

Clinical evaluation of ketoprofen (Orudis) in rheumatoid arthritis. Results of a multi-centre, double-blind, cross-over trial against phenylbutazone.

In a multi-centre, double-blind, cross-over trial comprising 38 patients with rheumatoid arthritis, ketoprofen was given at a dosage of 150 mg daily and phenylbutazone at a dosage of 300 mg daily, each for 2 weeks. On the basis of patient preference, general evaluation of the disease, morning stiffness, pain on movement and need for analgesics (dextropropoxyphene), it could be concluded that there was no significant difference between phenylbutazone and ketoprofene, although a tendency to more frequent and severe side-effects was seen with pehnylbutazone.

Clinical evaluation of keto profen (Orudis) in rheumatoid arthritis: results of a multi-centre double-blind trial against phenylbutazone.

In a double-blind cross-over trial in rheumatoid arthritis, no difference was found between ketoprofen and phenylbutazone with regard to clinical efficacy at the dosages used. There was a higher incidence of side-effects reported during treatment with phenylbutazone.

Interaction of indomethacin and acetylsalicylic acid as shown by the serum concentrations of indomethacin and salicylate.

A clinical-pharmacological study was performed to determine the effect of acetylsalicylic acid upon the serum concentration of indomethacin. 14 rheumatic patients were given indomethacin orally (25 mg X 4 for 4 days) and concurrently acetylsalicylic acid 3.7 g orally (0.9 g X 3 and 1.0 g X 1 daily), and 21 rheumatic patients were given indomethacin rectally in the morning (100 mg X 1) and concurrently acetylsalicylic acid 3.7 g orally (0.9 g X 3 and 1.0 g X 1 daily). On comparison with treatment with oral or rectal indomethacin alone, it was found that peak serum concentrations of indomethacin were significantly reduced (1% level), the times of the peaks were not shifted, and the areas beneath the serum concentration curves of indomethacin were smaller, but significantly so only if compared with rectal administration. In 12 rheumatic patients given indomethacin by rectum in the evening (100 mg X 1) and concurrently acetylsalicylic acid 3.7 g (0.9 g X 3 and 1.0 g X 1 daily), the serum level of indomethacin on the following morning (after 11 h) did not differ from that found after rectal treatment. A statistically but not biologically significant difference was observed between the mean serum half-lives of indomethacin given orally and rectally. For unknown reasons, concurrent doses of acetylsalicylic acid and indomethacin made the mean serum half-life of indomethacin longer than after its oral administration, but shorter than when the same dose of indomethacin was given rectally. There was no difference between serum levels of salicylate after oral administration of acetylsalicylic acid alone or after a concurrent oral or rectal dose of indomethacin. The results have been related to those reported previously, with respect to the interaction between indomethacin and acetylsalicylic acid, the serum levels of indomethacin after oral and rectal dosing, and the serum half-life of indomethacin based upon a one- or two-compartment model. The clinical relevance of the study is discussed.