Uterine artery embolisation for symptomatic adenomyosis with polyzene F-coated hydrogel microspheres: three-year clinical follow-up using UFS-QoL questionnaire.

PURPOSE: This study was designed to assess midterm outcome of uterine artery embolisation (UAE) for women with therapy-resistant adenomyosis using polyzene F-coated hydrogel microspheres. METHODS: Between September 2006 and January 2010, 29 consecutive women with adenomyosis (15 in combination with fibroids) were treated with UAE using polyzene F-coated hydrogel microspheres. Junction zone thickness was assessed with MRI at baseline and 3 months. Women filled out the uterine fibroid symptom and quality of life questionnaire at baseline, 3 months and after a mean clinical follow-up of 37 months (median 35, range 29-64 months). RESULTS: At baseline, symptom severity score of 29 women was mean 67 (median 72, range 23-100). At 3 months, this score decreased to mean 22 (median 15, range 0-66) and mean 15 (median 17, range 0-34) at final follow-up. At final follow-up of mean 37 months (median 35, range 29-64 months), 22 of 29 (76 %) patients were asymptomatic. Of these 22 women, 3 underwent a second UAE at 6, 7, and 14 months. The remaining seven patients clinically improved but still had symptoms; one underwent a hysterectomy. There was no difference in outcome between women with pure adenomyosis and women with additional fibroids. The junction zone of 4 women with additional therapy was significantly thicker compared with the remaining 25 patients. CONCLUSIONS: In women with therapy resistant adenomyosis, UAE using polyzene F-coated hydrogel microspheres resulted in 3 years preservation of the uterus in 28 of 29 (97 %) with good clinical outcome in the vast majority of patients. Initial thickness of the junction zone is related to additional therapy.

Effect of chronic mixed pesticide exposure on peripheral and autonomic nerve function.

In a cross-sectional study involving 131 flower bulb farmers (mean age = 43 y) and 67 well-matched controls, peripheral and autonomic nerve functions were examined. The study group had been exposed during a period of 20 y (standard deviation = 7) and applied a similar pesticide package. Lifetime cumulative exposure was estimated based on exposure levels for specific application methods and duration of exposure. Exposure-related decreased conduction velocities were found in the motor fibers of the median (-1.1 m/s) and peroneal (fast fibers: -1.2 m/s, slow fibers: -1.3 m/s) nerves, and in the sensory fibers of the median (-1.4 m/s) and sural (-0.9 m/s) nerves. In addition, the refractory period was determined and found to be increased in the sural and peroneal nerves. With regard to the autonomic nerve function, a decrease was found in resting sinus arrhythmia (-10%).

Metabolic activation of 1,2,4-trichlorobenzene and pentachlorobenzene by rat liver microsomes: a major role for quinone metabolites.

Microsomal metabolism of 1,2,4-[14C]trichlorobenzene (1,2,4-TrCB) and [14C]pentachlorobenzene (PeCB) was studied with special emphasis on the conversion-dependent covalent binding to protein and DNA. 1,2,4-TrCB was metabolized to 2,3,6- and 2,4,5-trichlorophenol, and to a lesser extent to 2,4,6- and 2,3,5-trichlorophenol, and trichlorohydroquinone. About 10% of all metabolites became covalently bound to protein in a rather nonselective way. For 1,2,4-TrCB and PeCB a strong correlation between secondary metabolism to hydroquinones and covalent binding was established. Protein binding was completely inhibited by the addition of ascorbic acid, indicating quinone metabolites as the sole reactive species formed. Both 1,2,4-TrCB and PeCB alkylated DNA, although to a much lesser extent than protein (0.5 and 0.3% of all metabolites, respectively). Nonquinone intermediates, presumably epoxides, were responsible for a minor portion of the observed DNA binding, since complete inhibition by ascorbic acid was not reached. The differential role of cytochrome P450 both in primary and in secondary metabolism was demonstrated by the use of microsomes from rats pretreated with different inducers. Dexamethasone (DEX) microsomes (cytochrome P450IIIA1) showed the highest activity toward these chlorinated benzenes (14 nmol/mg/5 min for 1,2,4-TrCB and 36 nmol/mg/10 min for PeCB, both with regard to the formation of phenols and to the formation of protein-bound metabolites. In addition, DEX microsomes preferentially formed 2,3,6-trichlorophenol, whereas other microsomal suspensions formed 2,4,5-trichlorophenol as the major isomer. The present study clearly demonstrates the high alkylating potency of secondary quinone metabolites derived from chlorinated benzenes and poses a need for reevaluation of the role of epoxides in the observed toxicity of these compounds.