Osteoporotic risk and physeal closure in prepubertal ovariohysterectomized cats.

We aimed to examine the early effects of prepubertal ovariohysterectomy (P-OHE) on bone loss and proximal physeal closure in cats. Fourteen kittens randomly underwent P-OHE or sham operations (S-OP) at three months (mo) of age and were allocated to group I and group II. Each mo between four and nine mo of age, dual-energy X-ray absorptiometry (DEXA) scans were performed to determine the total body bone mineral density (BMD) and bone mineral content (BMC). Proximal radial physeal closure and radial length were determined by radiography. Bone-specific alkaline phosphatase (BAP), carboxy-terminal collagen teleopeptide (CTX), 17-ß estradiol, progesterone, calcium (Ca) and phosphorus (P) were measured in the serum samples. No significant differences were observed between the groups in terms of BMD, BMC, BAP, BAP/CTX, P, progesterone and body weight (BW) (between 4 and 9mo) and for Ca (between 5 and 9mo) and for CTX levels (between 4 and 8mo). The 17-ß estradiol was significantly higher at 6, 8 and 9mo of age in the S-OP group due to puberty (P=0.02, P=0.03 and P=0.02 respectively). Although there was a significant difference (P=0.0002) between the P-OHE and S-OP groups in terms of the proximal radial physeal closure times (7.43±0.20mo and 6.14±0.14mo, respectively), no significant difference was observed for the mean radius length (10.59±0.10cm and 10.06±0.27cm, respectively) at the last evaluation time. In conclusion, prepubertal ovariohysterectomized cats do not have any osteoporotic risks until nine mo of age and exhibit a delayed physeal closure time without a change in radius length.

The evaluation of endothelin 1 (EDN1) and endothelin receptor type A (EDNRA) gene polymorphisms in Hashimoto's thyroiditis.

PURPOSE: Endothelin1 (EDN1) is well established marker of inflammation. The functions of EDN1 are mediated mainly by endothelin receptors type A (EDNRA). The etiopathogenesis of Hashimoto's thyroiditis (HT) remains still elusive although the role of chronic inflammation and subsequent endothelial dysfunction has been established. This study examined firstly the possible association of EDN1 (G5665Tand T-1370G) and EDNRA (C+70G and G-231A) single nucleotide polymorphisms (SNPs) with the occurrence of HT, and evaluates the relationship between genotypes and clinical/laboratory manifestation of HT. MATERIALS AND METHODS: We analyzed genotype and allele distributions of above mentioned polymorphisms in 163 patients with HT and 181 healthy controls by real-time PCR combined with melting curve analysis. RESULTS: No significant associations between HT and variant alleles of EDN1 5665 and -1370, as well as EDNRA +70 and -231 SNPs were found. Haplotype analysis demonstrated that there was a strong (D'=0.76, r(2)=0.487) and weak (D'=0.403, r(2)=0.086) linkage disequilibrium (LD) between EDN1 -1370 and 5665, and between EDNRA -231 and +70 SNPs, respectively. However, haplotype frequencies in patients were similar to those in controls. In addition, it was observed that the EDNRA +70 G allele had protective effect against early (at age before 40 years) disease onset of HT (OR: 0.51, 95% CI=0.32-0.79, p=0.003). CONCLUSION: Although no significant associations between susceptibility to HT with EDN1 5665 and -1370, as well as with EDNRA+70 and -231 SNPs were found, EDNRA +70 polymorphism was related with decreased risk for early onset HT.