Bongsuk Shim

A Retrospective Study of the Management of Vulvodynia

Purpose Vulvodynia is characterized by chronic vulvar pain caused by sexual intercourse and often results in female sexual dysfunction. Because the causes of vulvodynia are not clear, many patients do not receive optimal treatment. Recently, gabapentin and botulinum toxin A have both been shown to be effective treatments for vulvodynia. In this study, we retrospectively analyzed the clinical outcomes of botulinum toxin A and gabapentin treatment for chronic pain in women with this condition. Materials and Methods Seventy-three women with vulvar pain were administered either gabapentin (n=62) or botulinum toxin A (n=11) injections. Effectiveness was measured by use of a visual analogue scale (VAS). We analyzed the treatment method, treatment duration, success of treatment, and side effects or adverse reactions. Results Pain levels in both groups significantly decreased after treatment. In the gabapentin group, the VAS score decreased from 8.6 before treatment to 3.2 after treatment (p<0.001). The VAS score in the botulinum toxin A group was reduced from 8.1 to 2.5 (p<0.001). Side effects for both therapies were few and subsided with treatment with general antibiotics and nonsteroidal antiinflammatory drugs. Conclusions Gabapentin and botulinum toxin A are safe and effective treatments for vulvodynia. This condition can cause sexual dysfunction and affect quality of life. However, with proper management, satisfactory outcomes for women with vulvodynia can be achieved.

The Prostate Cancer Patient Had Higher C-Reactive Protein Than BPH Patient

Purpose C-reactive protein (CRP) is a general marker for inflammation and it has been associated with prostate cancer. We hypothesized that a correlation may exist between CRP and prostate cancer in patients undergoing transrectal biopsy of the prostate because of rising prostate-specific antigen (PSA) levels. Materials and Methods From January 2009 to March 2012, we retrospectively reviewed 710 patients who visited our urology department and were diagnosed as having a PSA value over 4.0 ng/mL. Patients with acute infections, rheumatoid arthritis, gout, asthma, chronic lung disease, myocardial infarction, or apoplexy and those who had taken nonsteroidal anti-inflammatory drugs were exempted from the research because these variables could have impacted CRP. After we applied the exclusion criteria, we selected 63 patients with prostate cancer and 140 patients with benign prostatic hyperplasia (BPH). Results A total of 203 patients were observed: 140 patients had BPH, and 63 patients had prostate cancer. Prostate cancer patients were divided into two groups by tumor-node-metastasis classification. The patients below T2 were group A, and those above T3 were group B. The natural logarithm of C-reactive protein (lnCRP) differed between the BPH group and the prostate cancer group. The lnCRP also differed between the BPH group and prostate cancer groups A and B (p<0.05). Conclusions The serum CRP level of the prostate cancer group was higher than that of the BPH group. Inflammation may be correlated with prostate cancer according to the serum CRP level.

MP44-15 ANXA10 AND ATP7A ARE THE MTOR PATHWAY DOWNSTREAM TO PREDICT THE RECURRENCE AND PROGRESSION IN NON-MUSCLE INVASIVE HIGH GRADE UROTHELIAL CARCINOMA OF THE BLADDER

Methylation of a CpG island of the miR200b gene was assessed by bisulfite-pyrosequencing. BCa cells were treated with the DNA demethylating agent 5-aza-20-deoxycytidine (5-aza-dC) to restore the expression of miR-200b. RESULTS: Of the 754 miRNAs analyzed, miR-200b was downregulated in CDDP-resistant BCa cells (Figure 1). Induction of miR-200b in T24RC cells restored the CDDP sensitivity (Figure 2a). In contrast, inhibition of miR-200b increased CDDP resistance in T24 and EJ138 cells (Figure 2b and 2c). The levels of methylation in the CpG islands of miR-200b were significantly increased in T24RC and EJ138RC as compared to their parental cells (T24RC, 83.3%; T24, 53.3%; EJ138RC, 77.0%; EJ138, 62.6%; P < 0.01, Student t test), and treatment with 5-aza-dC restored the miR-200b expression in resistant cells (Figure 3a and 3b). Moreover, treatment with CDDP and 5-aza-dC synergistically inhibited the growth of T24RC cells (Figure 3c). CONCLUSIONS: Our results suggest that epigenetic downregulation of miR-200b may be causally related to the CDDP-resistance in BCa, and that it could be a potential therapeutic target.