Side-effects of extracorporeal shock wave therapy (ESWT) in the treatment of tennis elbow.

Apart from a few observational reports, there are no studies on the side-effects of extracorporeal shock wave therapy (ESWT) in the treatment of insertion tendopathies. Within the framework of a randomised, placebo-controlled, single-blind, multicentre study to test the effectiveness of ESWT in the case of lateral epicondylitis (LE), side-effects were systematically recorded. A total of 272 patients from 15 centres was allocated at random to active ESWT (3 x 2000 pulses, energy flux density ED(+) 0.04 to 0.22 mJ/mm(2) under local anaesthesia) or placebo ESWT. In all, 399 ESWT and 402 placebo treatments were analysed. More side-effects were documented in the ESWT group (OR = 4.3, CI = [2.9; 6.3]) than in the placebo group. Most frequently, transitory reddening of the skin (21.1%), pain (4.8%) and small haematomas (3.0%) were found. Migraine was registered in four and syncopes in three instances after ESWT. ESWT for LE with an energy flux density of ED(+) 0.04 to 0.22 mJ/mm(2) is a treatment method which has very few side-effects. The possibility of migraine being triggered by ESWT and the risk of a syncope should be taken into account in the future. No physical shock wave parameters could be definitely identified as the cause of the side-effects observed.

Further evidence for linkage of low-mid frequency hearing impairment to the candidate region on chromosome 4p16.3.

We have investigated a three-generation family with an autosomal dominant low-mid frequency hearing loss. Audiograms show consistently a hearing threshold of 50+/-20 db hearing loss (HL) between 250 Hz and 1-2 kHz. Normal hearing level was reached between 3 and 6 kHz in all examined children. Adult patients show an additional hearing impairment (HI) in the mid and higher frequencies that seems to differ from presbyacusis. The HI is always bilateral and symmetrical. Genes causing non-syndromic autosomal-dominant deafness with HI in the low and mid frequencies were previously mapped to chromosome 4p16.3 (DFNA6, DFNA14) and chromosome 5q31 (DFNA1). After exclusion of linkage to DFNA1 on chromosome 5, we mapped the candidate gene region to the DFNA14 and DFNA6 loci, between the genetic markers D4S432 and D4S431, located on chromosome 4. This is a further family in which evident linkage of low-mid frequency HI to the candidate region on chromosome 4p16.3 has been found.

A bivariate Haseman-Elston method and application to the analysis of asthma-related phenotypes on chromosome 5q.

We propose a bivariate combination of different Haseman-Elston (HE) methods for model free linkage analysis of quantitative traits. Adjustments for correlations of phenotypes and sibship sizes > 2 are performed using generalized estimating equations (GEE). All calculations are carried out with freely available software packages. We illustrate the application of standard HE methods, the unified HE method, and our novel approach to asthma-associated quantitative traits from the COAG-Perth data set [Palmer et al., 1998, Am J Respir Crit Care Med 158:1825-30]. Our multipoint analyses provide evidence for linkage between log IgE levels adjusted for age, gender and antigen-specific IgE titers. Our results are consistent with previous findings that suggest the existence of loci regulating asthma-associated quantitative traits in the 5q31-33 chromosomal region. Simulation studies are required to compare the power of our novel bivariate HE with other HE approaches and the variance component method.

The use of sequential designs in genome scans for asthma susceptibility loci with affected sib pairs.

We use optimized group sequential study designs to analyze data from two genome scans (German and CSGA) for asthma susceptibility loci with affected sib pairs from Genetic Analysis Workshop (GAW) 12. Results are compared with those from a fixed sample design and the sequential probability ratio test (SPRT). The SPRT does not reach significance at any position. Using the fixed sample design, evidence for linkage is found on chromosomes 6 and 9 in the German and on chromosome 1 in the CSGA scan. The group sequential designs identify the same regions on chromosomes 1 and 6 with a reduced sample size.