Efficiency and costs of medical exercise therapy, conventional physiotherapy, and self-exercise in patients with chronic low back pain. A pragmatic, randomized, single-blinded, controlled trial with 1-year follow-up.

STUDY DESIGN: A multicenter, randomized, single-blinded controlled trial with 1-year follow-up. OBJECTIVES: To evaluate the efficiency of progressively graded medical exercise therapy, conventional physiotherapy, and self-exercise by walking in patients with chronic low back pain. SUMMARY AND BACKGROUND DATA: Varieties of medical exercise therapy and conventional physiotherapy are considered to reduce symptoms, improve function, and decrease sickness absence, but this opinion is controversial. METHODS: Patients with chronic low back pain or radicular pain sick-listed for more than 8 weeks and less than 52 weeks (Sickness Certificate II) were included. The treatment lasted 3 months (36 treatments). Pain intensity, functional ability, patient satisfaction, return to work, number of days on sick leave, and costs were recorded. RESULTS: Of the 208 patients included in this study, 71 were randomly assigned to medical exercise therapy, 67 to conventional physiotherapy, and 70 to self-exercise. Thirty-three (15.8%) patients dropped out during the treatment period. No difference was observed between the medical exercise therapy and conventional physiotherapy groups, but both were significantly better than self-exercise group. Patient satisfaction was highest for medical exercise therapy. Return to work rates were equal for all 3 intervention groups at assessment 15 months after therapy was started, with 123 patients were back to work. In terms of costs for days on sick leave, the medical exercise therapy group saved 906,732 Norwegian Kroner (NOK) ($122,531.00), and the conventional physiotherapy group saved NOK 1,882,560 ($254,200.00), compared with the self-exercise group. CONCLUSIONS: The efficiency of medical exercise therapy and conventional physiotherapy is shown. Leaving patients with chronic low back pain untampered poses a risk of worsening the disability, resulting in longer periods of sick leave.

Application of natural and amplification created restriction sites for the diagnosis of PKU mutations.

PCR amplification, either conventional, or as site directed mutagenesis using primers with mismatched 3'-ends, followed by restriction endonuclease digestion, provides rapid, non-isotope assays of known mutations in the human phenylalanine hydroxylase gene. Such assays were shown to have the potential to detect all of the 18 presently reported phenylketonuria mutations. The practical applicability of this approach was demonstrated for eight mutations in Norwegian phenylketonuria patients, among them the most common ones.

A termination mutant prevalent in Norwegian haplotype 7 phenylketonuria genes.

RFLPs in the phenylalanine hydroxylase (PAH) gene locus were determined in 47 Norwegian nuclear families that had at least one child with phenylketonuria (PKU). The PKU haplotype distribution differed somewhat from that of other European populations. Mutant haplotype 7 is relatively rare in other populations but constituted 20% of all mutant haplotypes in Norway. In 14 of the 17 mutant haplotypes 7, a previously unreported deletion of the BamHI restriction site in exon 7 of the PAH gene was observed. The abrogation of the BamHI site was shown to be due to a G-to-T transversion, changing Gly 272 to Ter 272 in exon 7 of the gene, thus directly identifying the PKU mutation. Unlike the families of the other PKU patients, the families with this mutation clustered along the southeastern coast of Norway, suggesting a founder effect for this mutation.